Component

Silica and soluble silicon

A collection spanning soluble silicon chemistry and silica particles. Orthosilicic acid transport, connective-tissue responses and particle injury retain separate molecular identities, routes and experimental exposures.

67 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

Human evidence only

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

Where it participates (unsigned role)

Orthosilicic acid in water did not significantly increase endogenous aluminum excretion over 32 hours in five volunteers.
Orthosilicic acid / Si(OH)4 → Human urinary aluminum excretion source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Water dosing, small human kinetic study.
limitations
Different matrix, baseline aluminum and timing may matter; urinary output is not a measurement of brain aluminum.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
A separate human study did not reproduce increased aluminum clearance.
primary_references
Silicic acid: its gastrointestinal uptake and urinary excretion in man and effects on aluminium excretion. · 1999 · https://pubmed.ncbi.nlm.nih.gov/10612067/ · DOI 10.1016/s0162-0134(99)00126-9
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 112–118
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Water dosing, small human kinetic study. · source_derived_draft · unverified_draft
## silica-aluminum-urine-null A separate human study did not reproduce increased aluminum clearance. Orthosilicic acid in water did not significantly increase endogenous aluminum excretion over 32 hours in five volunteers. Model: Water dosing, small human kinetic study. Limitations: Different matrix, baseline aluminum and timing may matter; urinary output is not a measurement of brain aluminum. Evidence access: Primary abstract Silicic acid: its gastrointestinal uptake and urinary excretion in man and effects on aluminium excretion. · 1999 · https://pubmed.ncbi.nlm.nih.gov/10612067/ · DOI 10.1016/s0162-0134(99)00126-9
Complete structured claim and evidence
Beer-derived monosilicic acid ingestion was accompanied by increased urinary aluminum in this study.
Orthosilicic acid / Si(OH)4 → Human urinary aluminum excretion source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Healthy volunteers; beverage matrix and isotope experiments.
limitations
Kidney-lumen complex formation and reduced reabsorption were proposed, not directly established molecular targets.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
A renal effect was proposed in addition to intestinal binding.
primary_references
The role of silicic acid in the renal excretion of aluminium. · 1996 · https://pubmed.ncbi.nlm.nih.gov/8726215/
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 104–110
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Healthy volunteers; beverage matrix and isotope experiments. · source_derived_draft · unverified_draft
## silica-aluminum-urine-positive A renal effect was proposed in addition to intestinal binding. Beer-derived monosilicic acid ingestion was accompanied by increased urinary aluminum in this study. Model: Healthy volunteers; beverage matrix and isotope experiments. Limitations: Kidney-lumen complex formation and reduced reabsorption were proposed, not directly established molecular targets. Evidence access: Primary abstract The role of silicic acid in the renal excretion of aluminium. · 1996 · https://pubmed.ncbi.nlm.nih.gov/8726215/
Complete structured claim and evidence
Combined AQP3/AQP7/AQP9/AQP10 RNA interference reduced silicon efflux from preloaded HEK-293 cells.
Combined human aquaglyceroporin silencing → Silicon efflux from human HEK-293 cells source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary full text
experimental_model
Human HEK-293 cells, 2 mM loading and brief efflux assay.
limitations
Combined knockdown does not quantify each channel’s independent in-vivo contribution.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
Loss of transport machinery changes silicon movement.
primary_references
Aquaporins Mediate Silicon Transport in Humans. · 2015 · https://pubmed.ncbi.nlm.nih.gov/26313002/ · DOI 10.1371/journal.pone.0136149
trigger_kind
machinery_impairment Imported condition classification; unverified.
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 48–54
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human HEK-293 cells, 2 mM loading and brief efflux assay. · source_derived_draft · unverified_draft
## silica-aqp-silencing Loss of transport machinery changes silicon movement. Combined AQP3/AQP7/AQP9/AQP10 RNA interference reduced silicon efflux from preloaded HEK-293 cells. Model: Human HEK-293 cells, 2 mM loading and brief efflux assay. Limitations: Combined knockdown does not quantify each channel’s independent in-vivo contribution. Evidence access: Primary full text Aquaporins Mediate Silicon Transport in Humans. · 2015 · https://pubmed.ncbi.nlm.nih.gov/26313002/ · DOI 10.1371/journal.pone.0136149
Complete structured claim and evidence
Expression of human AQP10 increased silicon transport in the tested oocyte and HEK-293 systems.
Human aquaporin 10 / AQP10 → Orthosilicic acid / Si(OH)4 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Human constructs in Xenopus oocytes and human HEK-293 cells.
limitations
Expression-system flux does not establish the dominant transporter in every human tissue.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
AQP10 provides a separately identifiable route for soluble silicon.
primary_references
Aquaporins Mediate Silicon Transport in Humans. · 2015 · https://pubmed.ncbi.nlm.nih.gov/26313002/ · DOI 10.1371/journal.pone.0136149
transport_effect
raises Expression increased silicon transport in the oocyte and HEK-293 uptake systems.
transport_pool
the expressing cell Expression increased silicon transport in the oocyte and HEK-293 uptake systems.
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 40–46
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human constructs in Xenopus oocytes and human HEK-293 cells. · source_derived_draft · unverified_draft
## silica-aqp10-transport AQP10 provides a separately identifiable route for soluble silicon. Expression of human AQP10 increased silicon transport in the tested oocyte and HEK-293 systems. Model: Human constructs in Xenopus oocytes and human HEK-293 cells. Limitations: Expression-system flux does not establish the dominant transporter in every human tissue. Evidence access: Primary full text Aquaporins Mediate Silicon Transport in Humans. · 2015 · https://pubmed.ncbi.nlm.nih.gov/26313002/ · DOI 10.1371/journal.pone.0136149
Complete structured claim and evidence
Expression of human AQP3 increased silicon transport in the tested oocyte and HEK-293 systems.
Human aquaporin 3 / AQP3 → Orthosilicic acid / Si(OH)4 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Human constructs in Xenopus oocytes and human HEK-293 cells.
limitations
Expression-system flux does not establish the dominant transporter in every human tissue.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
AQP3 provides a separately identifiable route for soluble silicon.
primary_references
Aquaporins Mediate Silicon Transport in Humans. · 2015 · https://pubmed.ncbi.nlm.nih.gov/26313002/ · DOI 10.1371/journal.pone.0136149
transport_effect
raises Expression increased silicon transport in the oocyte and HEK-293 uptake systems.
transport_pool
the expressing cell Expression increased silicon transport in the oocyte and HEK-293 uptake systems.
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 16–22
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human constructs in Xenopus oocytes and human HEK-293 cells. · source_derived_draft · unverified_draft
## silica-aqp3-transport AQP3 provides a separately identifiable route for soluble silicon. Expression of human AQP3 increased silicon transport in the tested oocyte and HEK-293 systems. Model: Human constructs in Xenopus oocytes and human HEK-293 cells. Limitations: Expression-system flux does not establish the dominant transporter in every human tissue. Evidence access: Primary full text Aquaporins Mediate Silicon Transport in Humans. · 2015 · https://pubmed.ncbi.nlm.nih.gov/26313002/ · DOI 10.1371/journal.pone.0136149
Complete structured claim and evidence
Expression of human AQP7 increased silicon transport in the tested oocyte and HEK-293 systems.
Human aquaporin 7 / AQP7 → Orthosilicic acid / Si(OH)4 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Human constructs in Xenopus oocytes and human HEK-293 cells.
limitations
Expression-system flux does not establish the dominant transporter in every human tissue.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
AQP7 provides a separately identifiable route for soluble silicon.
primary_references
Aquaporins Mediate Silicon Transport in Humans. · 2015 · https://pubmed.ncbi.nlm.nih.gov/26313002/ · DOI 10.1371/journal.pone.0136149
transport_effect
raises Expression increased silicon transport in the oocyte and HEK-293 uptake systems.
transport_pool
the expressing cell Expression increased silicon transport in the oocyte and HEK-293 uptake systems.
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 24–30
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human constructs in Xenopus oocytes and human HEK-293 cells. · source_derived_draft · unverified_draft
## silica-aqp7-transport AQP7 provides a separately identifiable route for soluble silicon. Expression of human AQP7 increased silicon transport in the tested oocyte and HEK-293 systems. Model: Human constructs in Xenopus oocytes and human HEK-293 cells. Limitations: Expression-system flux does not establish the dominant transporter in every human tissue. Evidence access: Primary full text Aquaporins Mediate Silicon Transport in Humans. · 2015 · https://pubmed.ncbi.nlm.nih.gov/26313002/ · DOI 10.1371/journal.pone.0136149
Complete structured claim and evidence
Phloretin increased AQP9-mediated silicon influx under the tested hypoosmolar conditions while inhibiting water transport.
Phloretin → Human aquaporin 9 / AQP9 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Human AQP9 in Xenopus oocytes; 0.1 mM phloretin, 2 mM silicic acid.
limitations
Not a demonstrated food interaction; the abstract’s phloretin-sensitive wording does not mean silicon flux was inhibited.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
A transport inhibitor can affect two substrates differently.
primary_references
Aquaporins Mediate Silicon Transport in Humans. · 2015 · https://pubmed.ncbi.nlm.nih.gov/26313002/ · DOI 10.1371/journal.pone.0136149
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 56–62
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human AQP9 in Xenopus oocytes; 0.1 mM phloretin, 2 mM silicic acid. · source_derived_draft · unverified_draft
## silica-aqp9-phloretin A transport inhibitor can affect two substrates differently. Phloretin increased AQP9-mediated silicon influx under the tested hypoosmolar conditions while inhibiting water transport. Model: Human AQP9 in Xenopus oocytes; 0.1 mM phloretin, 2 mM silicic acid. Limitations: Not a demonstrated food interaction; the abstract’s phloretin-sensitive wording does not mean silicon flux was inhibited. Evidence access: Primary full text Aquaporins Mediate Silicon Transport in Humans. · 2015 · https://pubmed.ncbi.nlm.nih.gov/26313002/ · DOI 10.1371/journal.pone.0136149
Complete structured claim and evidence
Expression of human AQP9 increased silicon transport in the tested oocyte and HEK-293 systems.
Human aquaporin 9 / AQP9 → Orthosilicic acid / Si(OH)4 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Human constructs in Xenopus oocytes and human HEK-293 cells.
limitations
Expression-system flux does not establish the dominant transporter in every human tissue.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
AQP9 provides a separately identifiable route for soluble silicon.
primary_references
Aquaporins Mediate Silicon Transport in Humans. · 2015 · https://pubmed.ncbi.nlm.nih.gov/26313002/ · DOI 10.1371/journal.pone.0136149
transport_effect
raises Expression increased silicon transport in the oocyte and HEK-293 uptake systems.
transport_pool
the expressing cell Expression increased silicon transport in the oocyte and HEK-293 uptake systems.
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 32–38
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human constructs in Xenopus oocytes and human HEK-293 cells. · source_derived_draft · unverified_draft
## silica-aqp9-transport AQP9 provides a separately identifiable route for soluble silicon. Expression of human AQP9 increased silicon transport in the tested oocyte and HEK-293 systems. Model: Human constructs in Xenopus oocytes and human HEK-293 cells. Limitations: Expression-system flux does not establish the dominant transporter in every human tissue. Evidence access: Primary full text Aquaporins Mediate Silicon Transport in Humans. · 2015 · https://pubmed.ncbi.nlm.nih.gov/26313002/ · DOI 10.1371/journal.pone.0136149
Complete structured claim and evidence
Ten micromolar orthosilicic acid increased BMP2 expression in human osteoblast-like cells.
Orthosilicic acid / Si(OH)4 → Human BMP2 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human MG-63/U2-OS cell program.
limitations
Expression change does not identify a direct silicon receptor.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
A bone-development signal increased after exposure.
primary_references
Biological Silicon Stimulates Collagen Type 1 and Osteocalcin Synthesis in Human Osteoblast-Like Cells Through the BMP-2/Smad/RUNX2 Signaling Pathway. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27025722/ · DOI 10.1007/s12011-016-0686-3
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 144–150
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human MG-63/U2-OS cell program. · source_derived_draft · unverified_draft
## silica-bmp-expression A bone-development signal increased after exposure. Ten micromolar orthosilicic acid increased BMP2 expression in human osteoblast-like cells. Model: Human MG-63/U2-OS cell program. Limitations: Expression change does not identify a direct silicon receptor. Evidence access: Primary abstract Biological Silicon Stimulates Collagen Type 1 and Osteocalcin Synthesis in Human Osteoblast-Like Cells Through the BMP-2/Smad/RUNX2 Signaling Pathway. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27025722/ · DOI 10.1007/s12011-016-0686-3
Complete structured claim and evidence
CA-074-Me reduced silica-triggered IL-1 beta release, supporting a cathepsin-sensitive step.
CA-074-Me treatment of silica-exposed mouse macrophages → Mouse IL-1 beta source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Mouse macrophages; 10 micromolar CA-074-Me.
limitations
Pharmacology alone does not establish unique cathepsin B necessity. Correction record: A 2026 author correction replaces an erroneously duplicated lower-left Fig. 8c micrograph with the retrieved original. This is a figure correction, not a scientific contradiction or retraction. https://www.nature.com/articles/s41590-026-02468-9
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
A lysosomal protease inhibitor reduced inflammatory output.
primary_references
Silica crystals and aluminum salts activate the NALP3 inflammasome through phagosomal destabilization. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18604214/ · DOI 10.1038/ni.1631
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 448–454
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse macrophages; 10 micromolar CA-074-Me. · source_derived_draft · unverified_draft
## silica-cathepsin-inhibitor A lysosomal protease inhibitor reduced inflammatory output. CA-074-Me reduced silica-triggered IL-1 beta release, supporting a cathepsin-sensitive step. Model: Mouse macrophages; 10 micromolar CA-074-Me. Limitations: Pharmacology alone does not establish unique cathepsin B necessity. Correction record: A 2026 author correction replaces an erroneously duplicated lower-left Fig. 8c micrograph with the retrieved original. This is a figure correction, not a scientific contradiction or retraction. https://www.nature.com/articles/s41590-026-02468-9 Evidence access: Primary full text Silica crystals and aluminum salts activate the NALP3 inflammasome through phagosomal destabilization. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18604214/ · DOI 10.1038/ni.1631
Complete structured claim and evidence
Cathepsin-B-deficient macrophages retained crystal-induced IL-1 beta release in this study.
Mouse cathepsin B → Mouse IL-1 beta source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Mouse bone-marrow macrophages with silica/MSU comparisons.
limitations
Compensation and other cathepsins remain possible; no universal dismissal of lysosomal injury.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
Genetic loss did not reproduce the inhibitor-based necessity claim.
primary_references
Activation of NLRP3 inflammasome by crystalline structures via cell surface contact. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25445147/ · DOI 10.1038/srep07281
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 472–478
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse bone-marrow macrophages with silica/MSU comparisons. · source_derived_draft · unverified_draft
## silica-cathepsin-knockout Genetic loss did not reproduce the inhibitor-based necessity claim. Cathepsin-B-deficient macrophages retained crystal-induced IL-1 beta release in this study. Model: Mouse bone-marrow macrophages with silica/MSU comparisons. Limitations: Compensation and other cathepsins remain possible; no universal dismissal of lysosomal injury. Evidence access: Primary full text Activation of NLRP3 inflammasome by crystalline structures via cell surface contact. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25445147/ · DOI 10.1038/srep07281
Complete structured claim and evidence
Silicon-deprived chicks showed abnormal epiphyseal cartilage and lower tibial hexosamine/collagen measures.
Low-silicon experimental chick diet → Endochondral bone growth in chicks source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Four-week cockerels on casein-based diets.
limitations
Developmental animal model, not a human nutritional threshold.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
Growing-animal cartilage was sensitive to the experimental diet.
primary_references
Biochemical and morphological changes associated with long bone abnormalities in silicon deficiency. · 1980 · https://pubmed.ncbi.nlm.nih.gov/7373430/ · DOI 10.1093/jn/110.5.1046
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 368–374
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Four-week cockerels on casein-based diets. · source_derived_draft · unverified_draft
## silica-chick-cartilage Growing-animal cartilage was sensitive to the experimental diet. Silicon-deprived chicks showed abnormal epiphyseal cartilage and lower tibial hexosamine/collagen measures. Model: Four-week cockerels on casein-based diets. Limitations: Developmental animal model, not a human nutritional threshold. Evidence access: Primary abstract Biochemical and morphological changes associated with long bone abnormalities in silicon deficiency. · 1980 · https://pubmed.ncbi.nlm.nih.gov/7373430/ · DOI 10.1093/jn/110.5.1046
Complete structured claim and evidence
U18666A-induced cholesterol accumulation reduced silica-induced inflammasome activation in mouse alveolar macrophages.
Cholesterol → Lysosomal permeabilization in silica-exposed mouse macrophages source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Pharmacologically altered lysosomal cholesterol handling.
limitations
Not evidence that raising blood cholesterol or dietary cholesterol protects the lung.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
Membrane-lipid handling can modify the response to particles.
primary_references
Role of lysosomes in silica-induced inflammasome activation and inflammation in absence of MARCO. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25054161/ · DOI 10.1155/2014/304180
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 496–502
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Pharmacologically altered lysosomal cholesterol handling. · source_derived_draft · unverified_draft
## silica-cholesterol-lysosome Membrane-lipid handling can modify the response to particles. U18666A-induced cholesterol accumulation reduced silica-induced inflammasome activation in mouse alveolar macrophages. Model: Pharmacologically altered lysosomal cholesterol handling. Limitations: Not evidence that raising blood cholesterol or dietary cholesterol protects the lung. Evidence access: Primary full text Role of lysosomes in silica-induced inflammasome activation and inflammation in absence of MARCO. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25054161/ · DOI 10.1155/2014/304180
Complete structured claim and evidence
Orthosilicic acid at 10–20 micromolar increased type I collagen synthesis in human osteoblast-like cultures.
Orthosilicic acid / Si(OH)4 → Human type I collagen source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
MG-63, HCC1 and primary human marrow-derived osteoblast-like cells.
limitations
Cell-culture synthesis is not demonstrated human bone strength or fracture benefit.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
Bone-forming cells produced more collagen scaffold.
primary_references
Orthosilicic acid stimulates collagen type 1 synthesis and osteoblastic differentiation in human osteoblast-like cells in vitro. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12633784/ · DOI 10.1016/s8756-3282(02)00950-x
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 120–126
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · MG-63, HCC1 and primary human marrow-derived osteoblast-like cells. · source_derived_draft · unverified_draft
## silica-collagen-production Bone-forming cells produced more collagen scaffold. Orthosilicic acid at 10–20 micromolar increased type I collagen synthesis in human osteoblast-like cultures. Model: MG-63, HCC1 and primary human marrow-derived osteoblast-like cells. Limitations: Cell-culture synthesis is not demonstrated human bone strength or fracture benefit. Evidence access: Primary abstract Orthosilicic acid stimulates collagen type 1 synthesis and osteoblastic differentiation in human osteoblast-like cells in vitro. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12633784/ · DOI 10.1016/s8756-3282(02)00950-x
Complete structured claim and evidence
Type I collagen mRNA did not increase despite greater collagen synthesis in treated MG-63 cells.
Orthosilicic acid / Si(OH)4 → Type I collagen mRNA in human MG-63 cells source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human osteosarcoma-derived MG-63 cells.
limitations
Translation, processing and turnover were not all separately resolved.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
The measured effect was not simply more collagen-gene transcription.
primary_references
Orthosilicic acid stimulates collagen type 1 synthesis and osteoblastic differentiation in human osteoblast-like cells in vitro. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12633784/ · DOI 10.1016/s8756-3282(02)00950-x
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 128–134
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human osteosarcoma-derived MG-63 cells. · source_derived_draft · unverified_draft
## silica-collagen-transcript-null The measured effect was not simply more collagen-gene transcription. Type I collagen mRNA did not increase despite greater collagen synthesis in treated MG-63 cells. Model: Human osteosarcoma-derived MG-63 cells. Limitations: Translation, processing and turnover were not all separately resolved. Evidence access: Primary abstract Orthosilicic acid stimulates collagen type 1 synthesis and osteoblastic differentiation in human osteoblast-like cells in vitro. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12633784/ · DOI 10.1016/s8756-3282(02)00950-x
Complete structured claim and evidence
Thirty micromolar OSA improved HUVEC proliferation, migration and tube formation under high glucose.
Orthosilicic acid / Si(OH)4 → HUVEC function under high glucose source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human HUVEC high-glucose model.
limitations
Clinical diabetic wound efficacy is unestablished; accessed abstract lacks full dose-response and inhibitor details.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
A recent study tested an additional stress context.
primary_references
Orthosilicic Acid Promotes Diabetic Wound Healing Through the PI3 K/AKT/mTOR Signaling Pathway. · 2026 · https://pubmed.ncbi.nlm.nih.gov/40517214/ · DOI 10.1007/s12011-025-04670-6
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 336–342
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human HUVEC high-glucose model. · source_derived_draft · unverified_draft
## silica-diabetic-endothelium A recent study tested an additional stress context. Thirty micromolar OSA improved HUVEC proliferation, migration and tube formation under high glucose. Model: Human HUVEC high-glucose model. Limitations: Clinical diabetic wound efficacy is unestablished; accessed abstract lacks full dose-response and inhibitor details. Evidence access: Primary abstract Orthosilicic Acid Promotes Diabetic Wound Healing Through the PI3 K/AKT/mTOR Signaling Pathway. · 2026 · https://pubmed.ncbi.nlm.nih.gov/40517214/ · DOI 10.1007/s12011-025-04670-6
Complete structured claim and evidence
OSA improved skin-wound healing in db/db mice, with PI3K/Akt/mTOR involvement reported.
Orthosilicic acid / Si(OH)4 → Wound healing in db/db mice source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Diabetic db/db mice; primary abstract.
limitations
Route, formulation and complete mediation experiments require full-text follow-up; not human treatment evidence.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
The research included an animal wound outcome.
primary_references
Orthosilicic Acid Promotes Diabetic Wound Healing Through the PI3 K/AKT/mTOR Signaling Pathway. · 2026 · https://pubmed.ncbi.nlm.nih.gov/40517214/ · DOI 10.1007/s12011-025-04670-6
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 344–350
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Diabetic db/db mice; primary abstract. · source_derived_draft · unverified_draft
## silica-diabetic-mouse-wound The research included an animal wound outcome. OSA improved skin-wound healing in db/db mice, with PI3K/Akt/mTOR involvement reported. Model: Diabetic db/db mice; primary abstract. Limitations: Route, formulation and complete mediation experiments require full-text follow-up; not human treatment evidence. Evidence access: Primary abstract Orthosilicic Acid Promotes Diabetic Wound Healing Through the PI3 K/AKT/mTOR Signaling Pathway. · 2026 · https://pubmed.ncbi.nlm.nih.gov/40517214/ · DOI 10.1007/s12011-025-04670-6
Complete structured claim and evidence
Dimethylsilanediol had no discernible survival effect up to 50 micromolar and increased survival at higher tested doses.
Dimethylsilanediol → Human Saos-2 colony survival source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human osteoblast-like cell comparison.
limitations
Environmental silicone degradation product, not evidence that silicone polymers or supplements share this activity.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
An organosilicon compound produced a different cellular response.
primary_references
Divergent effects of orthosilicic acid and dimethylsilanediol on cell survival and adhesion in human osteoblast-like cells. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18755397/ · DOI 10.1016/j.jtemb.2008.02.001
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 208–214
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human osteoblast-like cell comparison. · source_derived_draft · unverified_draft
## silica-dimethyl-form An organosilicon compound produced a different cellular response. Dimethylsilanediol had no discernible survival effect up to 50 micromolar and increased survival at higher tested doses. Model: Human osteoblast-like cell comparison. Limitations: Environmental silicone degradation product, not evidence that silicone polymers or supplements share this activity. Evidence access: Primary abstract Divergent effects of orthosilicic acid and dimethylsilanediol on cell survival and adhesion in human osteoblast-like cells. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18755397/ · DOI 10.1016/j.jtemb.2008.02.001
Complete structured claim and evidence
Silicon-treated HUVECs increased catalase mRNA under the reported normal and peroxide conditions.
Sodium-metasilicate-derived soluble silicon culture preparation → Human catalase source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Human HUVECs, 0.5 mM silicon preparation.
limitations
Expression is not measured catalytic flux or proof that silicon replaces established metal cofactors.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
An individual antioxidant or vascular enzyme was measured.
primary_references
Ionic silicon improves endothelial cells' survival under toxic oxidative stress by overexpressing angiogenic markers and antioxidant enzymes. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30062712/ · DOI 10.1002/term.2744
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 304–310
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human HUVECs, 0.5 mM silicon preparation. · source_derived_draft · unverified_draft
## silica-endothelial-human-catalase An individual antioxidant or vascular enzyme was measured. Silicon-treated HUVECs increased catalase mRNA under the reported normal and peroxide conditions. Model: Human HUVECs, 0.5 mM silicon preparation. Limitations: Expression is not measured catalytic flux or proof that silicon replaces established metal cofactors. Evidence access: Primary full text Ionic silicon improves endothelial cells' survival under toxic oxidative stress by overexpressing angiogenic markers and antioxidant enzymes. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30062712/ · DOI 10.1002/term.2744
Complete structured claim and evidence
The 0.5 mM silicon preparation increased HIF1A expression in HUVECs with or without the tested peroxide challenge.
Sodium-metasilicate-derived soluble silicon culture preparation → HIF-1 alpha source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Human endothelial cultures; sodium-metasilicate-derived preparation.
limitations
Expression association does not establish direct activation or clinical angiogenesis.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
A distinct vascular regulator changed after exposure.
primary_references
Ionic silicon improves endothelial cells' survival under toxic oxidative stress by overexpressing angiogenic markers and antioxidant enzymes. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30062712/ · DOI 10.1002/term.2744
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 528–534
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human endothelial cultures; sodium-metasilicate-derived preparation. · source_derived_draft · unverified_draft
## silica-endothelial-marker-hif1a A distinct vascular regulator changed after exposure. The 0.5 mM silicon preparation increased HIF1A expression in HUVECs with or without the tested peroxide challenge. Model: Human endothelial cultures; sodium-metasilicate-derived preparation. Limitations: Expression association does not establish direct activation or clinical angiogenesis. Evidence access: Primary full text Ionic silicon improves endothelial cells' survival under toxic oxidative stress by overexpressing angiogenic markers and antioxidant enzymes. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30062712/ · DOI 10.1002/term.2744
Complete structured claim and evidence
The 0.5 mM silicon preparation increased VEGFR2 / KDR expression in HUVECs with or without the tested peroxide challenge.
Sodium-metasilicate-derived soluble silicon culture preparation → Human VEGFR2 / KDR source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Human endothelial cultures; sodium-metasilicate-derived preparation.
limitations
Expression association does not establish direct activation or clinical angiogenesis.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
A distinct vascular regulator changed after exposure.
primary_references
Ionic silicon improves endothelial cells' survival under toxic oxidative stress by overexpressing angiogenic markers and antioxidant enzymes. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30062712/ · DOI 10.1002/term.2744
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 544–550
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human endothelial cultures; sodium-metasilicate-derived preparation. · source_derived_draft · unverified_draft
## silica-endothelial-marker-human-kdr A distinct vascular regulator changed after exposure. The 0.5 mM silicon preparation increased VEGFR2 / KDR expression in HUVECs with or without the tested peroxide challenge. Model: Human endothelial cultures; sodium-metasilicate-derived preparation. Limitations: Expression association does not establish direct activation or clinical angiogenesis. Evidence access: Primary full text Ionic silicon improves endothelial cells' survival under toxic oxidative stress by overexpressing angiogenic markers and antioxidant enzymes. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30062712/ · DOI 10.1002/term.2744
Complete structured claim and evidence
The 0.5 mM silicon preparation increased VEGFA expression in HUVECs with or without the tested peroxide challenge.
Sodium-metasilicate-derived soluble silicon culture preparation → Human VEGFA source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Human endothelial cultures; sodium-metasilicate-derived preparation.
limitations
Expression association does not establish direct activation or clinical angiogenesis.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
A distinct vascular regulator changed after exposure.
primary_references
Ionic silicon improves endothelial cells' survival under toxic oxidative stress by overexpressing angiogenic markers and antioxidant enzymes. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30062712/ · DOI 10.1002/term.2744
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 536–542
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human endothelial cultures; sodium-metasilicate-derived preparation. · source_derived_draft · unverified_draft
## silica-endothelial-marker-human-vegfa A distinct vascular regulator changed after exposure. The 0.5 mM silicon preparation increased VEGFA expression in HUVECs with or without the tested peroxide challenge. Model: Human endothelial cultures; sodium-metasilicate-derived preparation. Limitations: Expression association does not establish direct activation or clinical angiogenesis. Evidence access: Primary full text Ionic silicon improves endothelial cells' survival under toxic oxidative stress by overexpressing angiogenic markers and antioxidant enzymes. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30062712/ · DOI 10.1002/term.2744
Complete structured claim and evidence
Silicon-treated HUVECs increased NOS3 mRNA under the reported normal and peroxide conditions.
Sodium-metasilicate-derived soluble silicon culture preparation → Human endothelial nitric oxide synthase / eNOS / NOS3 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Human HUVECs, 0.5 mM silicon preparation.
limitations
Expression is not measured catalytic flux or proof that silicon replaces established metal cofactors.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
An individual antioxidant or vascular enzyme was measured.
primary_references
Ionic silicon improves endothelial cells' survival under toxic oxidative stress by overexpressing angiogenic markers and antioxidant enzymes. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30062712/ · DOI 10.1002/term.2744
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 312–318
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human HUVECs, 0.5 mM silicon preparation. · source_derived_draft · unverified_draft
## silica-endothelial-nos3 An individual antioxidant or vascular enzyme was measured. Silicon-treated HUVECs increased NOS3 mRNA under the reported normal and peroxide conditions. Model: Human HUVECs, 0.5 mM silicon preparation. Limitations: Expression is not measured catalytic flux or proof that silicon replaces established metal cofactors. Evidence access: Primary full text Ionic silicon improves endothelial cells' survival under toxic oxidative stress by overexpressing angiogenic markers and antioxidant enzymes. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30062712/ · DOI 10.1002/term.2744
Complete structured claim and evidence
Silicon-treated HUVECs increased SOD1 mRNA under the reported normal and peroxide conditions.
Sodium-metasilicate-derived soluble silicon culture preparation → Human copper-zinc superoxide dismutase / SOD1 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Human HUVECs, 0.5 mM silicon preparation.
limitations
Expression is not measured catalytic flux or proof that silicon replaces established metal cofactors.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
An individual antioxidant or vascular enzyme was measured.
primary_references
Ionic silicon improves endothelial cells' survival under toxic oxidative stress by overexpressing angiogenic markers and antioxidant enzymes. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30062712/ · DOI 10.1002/term.2744
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 296–302
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human HUVECs, 0.5 mM silicon preparation. · source_derived_draft · unverified_draft
## silica-endothelial-sod1 An individual antioxidant or vascular enzyme was measured. Silicon-treated HUVECs increased SOD1 mRNA under the reported normal and peroxide conditions. Model: Human HUVECs, 0.5 mM silicon preparation. Limitations: Expression is not measured catalytic flux or proof that silicon replaces established metal cofactors. Evidence access: Primary full text Ionic silicon improves endothelial cells' survival under toxic oxidative stress by overexpressing angiogenic markers and antioxidant enzymes. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30062712/ · DOI 10.1002/term.2744
Complete structured claim and evidence
A 0.5 mM silicon preparation improved HUVEC viability during hydrogen-peroxide exposure.
Sodium-metasilicate-derived soluble silicon culture preparation → HUVEC survival during peroxide challenge source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Sodium-metasilicate-derived medium; 0.6 mM H2O2 challenge.
limitations
Authors label exposure Si4+; this is not a measured pool of free aqueous Si4+. Supraphysiological culture exposure.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
Dissolved preparation altered the response to oxidative stress.
primary_references
Ionic silicon improves endothelial cells' survival under toxic oxidative stress by overexpressing angiogenic markers and antioxidant enzymes. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30062712/ · DOI 10.1002/term.2744
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 288–294
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Sodium-metasilicate-derived medium; 0.6 mM H2O2 challenge. · source_derived_draft · unverified_draft
## silica-endothelial-survival Dissolved preparation altered the response to oxidative stress. A 0.5 mM silicon preparation improved HUVEC viability during hydrogen-peroxide exposure. Model: Sodium-metasilicate-derived medium; 0.6 mM H2O2 challenge. Limitations: Authors label exposure Si4+; this is not a measured pool of free aqueous Si4+. Supraphysiological culture exposure. Evidence access: Primary full text Ionic silicon improves endothelial cells' survival under toxic oxidative stress by overexpressing angiogenic markers and antioxidant enzymes. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30062712/ · DOI 10.1002/term.2744
Complete structured claim and evidence
Urinary recovery was approximately 43% for orthosilicic acid, 17% for choline-stabilized acid and 1% for colloidal silica in this comparison.
Choline-stabilized orthosilicic acid → Urinary silicon recovery after oral preparations source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Small crossover comparisons; colloidal silica n=3, other sources at least five.
limitations
Different preparations and dissolution; not proof that choline itself suppresses absorption or defines a cofactor.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
The same elemental amount need not deliver the same soluble exposure.
primary_references
The comparative absorption of silicon from different foods and food supplements. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19356271/ · DOI 10.1017/S0007114509311757
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 80–86
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Small crossover comparisons; colloidal silica n=3, other sources at least five. · source_derived_draft · unverified_draft
## silica-formulation-absorption The same elemental amount need not deliver the same soluble exposure. Urinary recovery was approximately 43% for orthosilicic acid, 17% for choline-stabilized acid and 1% for colloidal silica in this comparison. Model: Small crossover comparisons; colloidal silica n=3, other sources at least five. Limitations: Different preparations and dissolution; not proof that choline itself suppresses absorption or defines a cofactor. Evidence access: Primary abstract The comparative absorption of silicon from different foods and food supplements. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19356271/ · DOI 10.1017/S0007114509311757
Complete structured claim and evidence
Lumbar spine BMD did not significantly change; a femoral-neck signal arose in a post-hoc subgroup.
Choline-stabilized orthosilicic acid → Lumbar spine BMD during choline-stabilized OSA trial source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Same 12-month calcium/D3-background trial.
limitations
Post-hoc subgroup findings are exploratory; not independent replication.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
A matrix marker and bone-density outcome did not provide equivalent evidence.
primary_references
Choline-stabilized orthosilicic acid supplementation as an adjunct to calcium/vitamin D3 stimulates markers of bone formation in osteopenic females: a randomized, placebo-controlled trial. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18547426/ · DOI 10.1186/1471-2474-9-85
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 384–390
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Same 12-month calcium/D3-background trial. · source_derived_draft · unverified_draft
## silica-human-bmd-null A matrix marker and bone-density outcome did not provide equivalent evidence. Lumbar spine BMD did not significantly change; a femoral-neck signal arose in a post-hoc subgroup. Model: Same 12-month calcium/D3-background trial. Limitations: Post-hoc subgroup findings are exploratory; not independent replication. Evidence access: Primary abstract Choline-stabilized orthosilicic acid supplementation as an adjunct to calcium/vitamin D3 stimulates markers of bone formation in osteopenic females: a randomized, placebo-controlled trial. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18547426/ · DOI 10.1186/1471-2474-9-85
Complete structured claim and evidence
Human MARCO expression in CHO cells supported silica binding and apoptosis.
Human MARCO → Response of human-MARCO-transfected hamster cells source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human construct in Chinese hamster ovary cells.
limitations
Not direct observation of human lung exposure or a universal uptake route.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
A human receptor was tested in a nonhuman host cell.
primary_references
MARCO mediates silica uptake and toxicity in alveolar macrophages from C57BL/6 mice. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16984918/ · DOI 10.1074/jbc.M605229200
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 416–422
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human construct in Chinese hamster ovary cells. · source_derived_draft · unverified_draft
## silica-human-marco-binding A human receptor was tested in a nonhuman host cell. Human MARCO expression in CHO cells supported silica binding and apoptosis. Model: Human construct in Chinese hamster ovary cells. Limitations: Not direct observation of human lung exposure or a universal uptake route. Evidence access: Primary abstract MARCO mediates silica uptake and toxicity in alveolar macrophages from C57BL/6 mice. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16984918/ · DOI 10.1074/jbc.M605229200
Complete structured claim and evidence
PINP differed from placebo at 12 months in the 6- and 12-mg Si groups without a clear dose response.
Choline-stabilized orthosilicic acid → Serum PINP during choline-stabilized OSA trial source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
184 women randomized; 136 completed; all received 1,000 mg calcium and 20 micrograms D3 daily.
limitations
Marker result is not fracture prevention; attrition and multiple endpoints matter.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
A collagen-formation marker changed on top of calcium and vitamin D.
primary_references
Choline-stabilized orthosilicic acid supplementation as an adjunct to calcium/vitamin D3 stimulates markers of bone formation in osteopenic females: a randomized, placebo-controlled trial. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18547426/ · DOI 10.1186/1471-2474-9-85
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 376–382
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · 184 women randomized; 136 completed; all received 1,000 mg calcium and 20 micrograms D3 daily. · source_derived_draft · unverified_draft
## silica-human-pinp A collagen-formation marker changed on top of calcium and vitamin D. PINP differed from placebo at 12 months in the 6- and 12-mg Si groups without a clear dose response. Model: 184 women randomized; 136 completed; all received 1,000 mg calcium and 20 micrograms D3 daily. Limitations: Marker result is not fracture prevention; attrition and multiple endpoints matter. Evidence access: Primary abstract Choline-stabilized orthosilicic acid supplementation as an adjunct to calcium/vitamin D3 stimulates markers of bone formation in osteopenic females: a randomized, placebo-controlled trial. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18547426/ · DOI 10.1186/1471-2474-9-85
Complete structured claim and evidence
Prolyl hydroxylase inhibitors abolished the orthosilicic-acid-associated collagen increase.
Prolyl hydroxylase inhibition in human osteoblast-like cells → Collagen synthesis response to orthosilicic acid source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Human osteoblast-like cell inhibitor study.
limitations
Does not prove direct silicon binding or silicon as an obligatory enzyme cofactor.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
Intact collagen-processing machinery was needed for the response.
primary_references
Orthosilicic acid stimulates collagen type 1 synthesis and osteoblastic differentiation in human osteoblast-like cells in vitro. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12633784/ · DOI 10.1016/s8756-3282(02)00950-x
trigger_kind
machinery_impairment Imported condition classification; unverified.
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 136–142
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human osteoblast-like cell inhibitor study. · source_derived_draft · unverified_draft
## silica-hydroxylase-block Intact collagen-processing machinery was needed for the response. Prolyl hydroxylase inhibitors abolished the orthosilicic-acid-associated collagen increase. Model: Human osteoblast-like cell inhibitor study. Limitations: Does not prove direct silicon binding or silicon as an obligatory enzyme cofactor. Evidence access: Primary abstract Orthosilicic acid stimulates collagen type 1 synthesis and osteoblastic differentiation in human osteoblast-like cells in vitro. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12633784/ · DOI 10.1016/s8756-3282(02)00950-x
Complete structured claim and evidence
Leupeptin reduced the measured cathepsin-B signal without preventing the nanoparticle-associated pyroptosis response.
Leupeptin → Pyroptosis-associated response in mouse RAW-ASC cells source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Mouse RAW-ASC cells; 1 microgram/mL leupeptin.
limitations
Leupeptin is not cathepsin-B-specific; measured abundance is not a selective genetic activity test.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
A protease-inhibitor result also failed to establish cathepsin B necessity.
primary_references
Characterization of Cathepsin B in Mediating Silica Nanoparticle-Induced Macrophage Pyroptosis via an NLRP3-Dependent Manner. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35966002/ · DOI 10.2147/JIR.S371536
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 512–518
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse RAW-ASC cells; 1 microgram/mL leupeptin. · source_derived_draft · unverified_draft
## silica-leupeptin-null A protease-inhibitor result also failed to establish cathepsin B necessity. Leupeptin reduced the measured cathepsin-B signal without preventing the nanoparticle-associated pyroptosis response. Model: Mouse RAW-ASC cells; 1 microgram/mL leupeptin. Limitations: Leupeptin is not cathepsin-B-specific; measured abundance is not a selective genetic activity test. Evidence access: Primary full text Characterization of Cathepsin B in Mediating Silica Nanoparticle-Induced Macrophage Pyroptosis via an NLRP3-Dependent Manner. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35966002/ · DOI 10.2147/JIR.S371536
Complete structured claim and evidence
LY294002 reduced pathway signals and osteogenic markers during orthosilicic acid treatment.
LY294002 treatment of human osteoblast-like cells → Collagen synthesis response to orthosilicic acid source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Human osteoblast-like cultures.
limitations
LY294002 has off-target effects and is not an inhibitor specific to the entire PI3K–Akt–mTOR chain.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
The cell response was sensitive to PI3K-pathway blockade.
primary_references
Orthosilicic Acid Accelerates Bone Formation in Human Osteoblast-Like Cells Through the PI3K-Akt-mTOR Pathway. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30421162/ · DOI 10.1007/s12011-018-1574-9
trigger_kind
machinery_impairment Imported condition classification; unverified.
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 176–182
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human osteoblast-like cultures. · source_derived_draft · unverified_draft
## silica-ly294002-block The cell response was sensitive to PI3K-pathway blockade. LY294002 reduced pathway signals and osteogenic markers during orthosilicic acid treatment. Model: Human osteoblast-like cultures. Limitations: LY294002 has off-target effects and is not an inhibitor specific to the entire PI3K–Akt–mTOR chain. Evidence access: Primary abstract Orthosilicic Acid Accelerates Bone Formation in Human Osteoblast-Like Cells Through the PI3K-Akt-mTOR Pathway. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30421162/ · DOI 10.1007/s12011-018-1574-9
Complete structured claim and evidence
Phagocytosed silica caused lysosomal swelling and leakage in mouse macrophages.
Crystalline silica / quartz particles → Lysosomal permeabilization in silica-exposed mouse macrophages source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Mouse macrophage imaging of vesicular cargo redistribution.
limitations
Particle preparation and cellular priming matter. Correction record: A 2026 author correction replaces an erroneously duplicated lower-left Fig. 8c micrograph with the retrieved original. This is a figure correction, not a scientific contradiction or retraction. https://www.nature.com/articles/s41590-026-02468-9
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
Particles can damage the compartment that engulfs them.
primary_references
Silica crystals and aluminum salts activate the NALP3 inflammasome through phagosomal destabilization. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18604214/ · DOI 10.1038/ni.1631
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 424–430
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse macrophage imaging of vesicular cargo redistribution. · source_derived_draft · unverified_draft
## silica-lysosome-damage Particles can damage the compartment that engulfs them. Phagocytosed silica caused lysosomal swelling and leakage in mouse macrophages. Model: Mouse macrophage imaging of vesicular cargo redistribution. Limitations: Particle preparation and cellular priming matter. Correction record: A 2026 author correction replaces an erroneously duplicated lower-left Fig. 8c micrograph with the retrieved original. This is a figure correction, not a scientific contradiction or retraction. https://www.nature.com/articles/s41590-026-02468-9 Evidence access: Primary full text Silica crystals and aluminum salts activate the NALP3 inflammasome through phagosomal destabilization. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18604214/ · DOI 10.1038/ni.1631
Complete structured claim and evidence
MARCO-null alveolar macrophages showed greater lysosomal leakage and IL-1 beta/caspase-1 responses despite lower silica uptake.
Mouse MARCO → Lysosomal permeabilization in silica-exposed mouse macrophages source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary full text
experimental_model
Primary mouse macrophages; silica 100 micrograms/mL.
limitations
Receptor uptake and lysosomal resilience are separate functions; not a contradiction of uptake measurements.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
Less uptake did not necessarily mean less inflammation.
primary_references
Role of lysosomes in silica-induced inflammasome activation and inflammation in absence of MARCO. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25054161/ · DOI 10.1155/2014/304180
trigger_kind
machinery_impairment Imported condition classification; unverified.
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 488–494
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Primary mouse macrophages; silica 100 micrograms/mL. · source_derived_draft · unverified_draft
## silica-marco-lysosome-loss Less uptake did not necessarily mean less inflammation. MARCO-null alveolar macrophages showed greater lysosomal leakage and IL-1 beta/caspase-1 responses despite lower silica uptake. Model: Primary mouse macrophages; silica 100 micrograms/mL. Limitations: Receptor uptake and lysosomal resilience are separate functions; not a contradiction of uptake measurements. Evidence access: Primary full text Role of lysosomes in silica-induced inflammasome activation and inflammation in absence of MARCO. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25054161/ · DOI 10.1155/2014/304180
Complete structured claim and evidence
MARCO loss or antibody blockade prevented silica uptake and cytotoxicity in C57BL/6 alveolar macrophages.
Mouse MARCO → Silica uptake in mouse alveolar macrophages source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Primary mouse macrophages; receptor-null and antibody experiments.
limitations
Mouse strain matters: BALB/c uptake was not blocked by the same receptor antibodies.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
A scavenger receptor can gate particle entry.
primary_references
MARCO mediates silica uptake and toxicity in alveolar macrophages from C57BL/6 mice. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16984918/ · DOI 10.1074/jbc.M605229200
trigger_kind
machinery_impairment Imported condition classification; unverified.
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 408–414
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Primary mouse macrophages; receptor-null and antibody experiments. · source_derived_draft · unverified_draft
## silica-marco-uptake A scavenger receptor can gate particle entry. MARCO loss or antibody blockade prevented silica uptake and cytotoxicity in C57BL/6 alveolar macrophages. Model: Primary mouse macrophages; receptor-null and antibody experiments. Limitations: Mouse strain matters: BALB/c uptake was not blocked by the same receptor antibodies. Evidence access: Primary abstract MARCO mediates silica uptake and toxicity in alveolar macrophages from C57BL/6 mice. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16984918/ · DOI 10.1074/jbc.M605229200
Complete structured claim and evidence
Silicon-releasing microcarriers increased HIF1A expression and stabilization, attributed to reduced PHD2 activity in HUVECs.
Mesoporous silica microcarriers → HIF-1 alpha source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human endothelial cells; released silicon in the ppm range.
limitations
Accessed abstract does not establish direct inhibitor binding; HIF PHD2 differs from collagen prolyl hydroxylase.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
A biomaterial study implicated oxygen-sensing machinery.
primary_references
Promoting angiogenesis with mesoporous microcarriers through a synergistic action of delivered silicon ion and VEGF. · 2017 · https://pubmed.ncbi.nlm.nih.gov/27918936/ · DOI 10.1016/j.biomaterials.2016.11.053
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 272–278
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human endothelial cells; released silicon in the ppm range. · source_derived_draft · unverified_draft
## silica-microcarrier-hif A biomaterial study implicated oxygen-sensing machinery. Silicon-releasing microcarriers increased HIF1A expression and stabilization, attributed to reduced PHD2 activity in HUVECs. Model: Human endothelial cells; released silicon in the ppm range. Limitations: Accessed abstract does not establish direct inhibitor binding; HIF PHD2 differs from collagen prolyl hydroxylase. Evidence access: Primary abstract Promoting angiogenesis with mesoporous microcarriers through a synergistic action of delivered silicon ion and VEGF. · 2017 · https://pubmed.ncbi.nlm.nih.gov/27918936/ · DOI 10.1016/j.biomaterials.2016.11.053
Complete structured claim and evidence
Microcarriers releasing silicon and loaded VEGF increased endothelial migration and tubular networking.
Mesoporous silica microcarriers → Endothelial response to silicon/VEGF microcarriers source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human HUVECs; engineered local-release formulation.
limitations
Not evidence of oral silica/VEGF supplementation or a universal synergy.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
A tested growth-factor combination promoted vascular-cell behavior.
primary_references
Promoting angiogenesis with mesoporous microcarriers through a synergistic action of delivered silicon ion and VEGF. · 2017 · https://pubmed.ncbi.nlm.nih.gov/27918936/ · DOI 10.1016/j.biomaterials.2016.11.053
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 280–286
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human HUVECs; engineered local-release formulation. · source_derived_draft · unverified_draft
## silica-microcarrier-vegf A tested growth-factor combination promoted vascular-cell behavior. Microcarriers releasing silicon and loaded VEGF increased endothelial migration and tubular networking. Model: Human HUVECs; engineered local-release formulation. Limitations: Not evidence of oral silica/VEGF supplementation or a universal synergy. Evidence access: Primary abstract Promoting angiogenesis with mesoporous microcarriers through a synergistic action of delivered silicon ion and VEGF. · 2017 · https://pubmed.ncbi.nlm.nih.gov/27918936/ · DOI 10.1016/j.biomaterials.2016.11.053
Complete structured claim and evidence
Orthosilicic acid increased miR-146a during later osteogenic differentiation of human mesenchymal stromal cells.
Orthosilicic acid / Si(OH)4 → Human miR-146a source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human MSC microarray and qPCR experiments.
limitations
Late-stage association is distinct from identification of the upstream silicon sensor.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
A regulatory RNA connects exposure to cell-state change.
primary_references
Orthosilicic acid, Si(OH)4, stimulates osteoblast differentiation in vitro by upregulating miR-146a to antagonize NF-κB activation. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27163405/ · DOI 10.1016/j.actbio.2016.05.007
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 184–190
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human MSC microarray and qPCR experiments. · source_derived_draft · unverified_draft
## silica-mir146a A regulatory RNA connects exposure to cell-state change. Orthosilicic acid increased miR-146a during later osteogenic differentiation of human mesenchymal stromal cells. Model: Human MSC microarray and qPCR experiments. Limitations: Late-stage association is distinct from identification of the upstream silicon sensor. Evidence access: Primary abstract Orthosilicic acid, Si(OH)4, stimulates osteoblast differentiation in vitro by upregulating miR-146a to antagonize NF-κB activation. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27163405/ · DOI 10.1016/j.actbio.2016.05.007
Complete structured claim and evidence
The monomeric preparation did not significantly reduce aluminum availability in the same study.
Orthosilicic acid / Si(OH)4 → Aluminum(III) source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Same three-person human tracer experiment.
limitations
Chemical-form difference is not a scientific contradiction.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
Soluble monomers and oligomers do not behave identically.
primary_references
Oligomeric but not monomeric silica prevents aluminum absorption in humans. · 2000 · https://pubmed.ncbi.nlm.nih.gov/10731501/ · DOI 10.1093/ajcn/71.4.944
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 96–102
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Same three-person human tracer experiment. · source_derived_draft · unverified_draft
## silica-monomer-aluminum-null Soluble monomers and oligomers do not behave identically. The monomeric preparation did not significantly reduce aluminum availability in the same study. Model: Same three-person human tracer experiment. Limitations: Chemical-form difference is not a scientific contradiction. Evidence access: Primary abstract Oligomeric but not monomeric silica prevents aluminum absorption in humans. · 2000 · https://pubmed.ncbi.nlm.nih.gov/10731501/ · DOI 10.1093/ajcn/71.4.944
Complete structured claim and evidence
Anti-miR-146a suppressed differentiation in MC3T3 preosteoblasts in the silicate study.
Anti-miR-146a treatment in mouse MC3T3 cells → Mouse osteoblast differentiation source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Mouse MC3T3 cells; distinguish from the human MSC discovery assay.
limitations
Abstract does not resolve all species-specific downstream targets.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
Removing a regulatory RNA weakened bone-cell maturation.
primary_references
Orthosilicic acid, Si(OH)4, stimulates osteoblast differentiation in vitro by upregulating miR-146a to antagonize NF-κB activation. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27163405/ · DOI 10.1016/j.actbio.2016.05.007
trigger_kind
machinery_impairment Imported condition classification; unverified.
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 192–198
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse MC3T3 cells; distinguish from the human MSC discovery assay. · source_derived_draft · unverified_draft
## silica-mouse-antimir Removing a regulatory RNA weakened bone-cell maturation. Anti-miR-146a suppressed differentiation in MC3T3 preosteoblasts in the silicate study. Model: Mouse MC3T3 cells; distinguish from the human MSC discovery assay. Limitations: Abstract does not resolve all species-specific downstream targets. Evidence access: Primary abstract Orthosilicic acid, Si(OH)4, stimulates osteoblast differentiation in vitro by upregulating miR-146a to antagonize NF-κB activation. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27163405/ · DOI 10.1016/j.actbio.2016.05.007
Complete structured claim and evidence
A 0.1 mM silicon preparation increased C2C12 viability, migration and myotube formation.
Sodium-metasilicate-derived soluble silicon culture preparation → Myotube formation by mouse C2C12 cells source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Mouse C2C12 cultures; sodium-metasilicate-derived medium.
limitations
Not proof of human muscle regeneration after supplementation.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
The soluble-preparation findings extend beyond bone cells.
primary_references
Ionic Silicon Protects Oxidative Damage and Promotes Skeletal Muscle Cell Regeneration. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33419056/ · DOI 10.3390/ijms22020497
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 320–326
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse C2C12 cultures; sodium-metasilicate-derived medium. · source_derived_draft · unverified_draft
## silica-muscle-myotubes The soluble-preparation findings extend beyond bone cells. A 0.1 mM silicon preparation increased C2C12 viability, migration and myotube formation. Model: Mouse C2C12 cultures; sodium-metasilicate-derived medium. Limitations: Not proof of human muscle regeneration after supplementation. Evidence access: Primary full text Ionic Silicon Protects Oxidative Damage and Promotes Skeletal Muscle Cell Regeneration. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33419056/ · DOI 10.3390/ijms22020497
Complete structured claim and evidence
Silicon preparations at 0.1–2 mM attenuated peroxide-associated loss of viability and differentiation.
Sodium-metasilicate-derived soluble silicon culture preparation → Peroxide injury in mouse C2C12 cells source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Mouse muscle-cell culture, 24-hour challenge experiments.
limitations
Does not identify a direct antioxidant reaction or an in-vivo effective dose.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
Oxidative challenge changed the context in which protection was observed.
primary_references
Ionic Silicon Protects Oxidative Damage and Promotes Skeletal Muscle Cell Regeneration. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33419056/ · DOI 10.3390/ijms22020497
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 328–334
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse muscle-cell culture, 24-hour challenge experiments. · source_derived_draft · unverified_draft
## silica-muscle-peroxide Oxidative challenge changed the context in which protection was observed. Silicon preparations at 0.1–2 mM attenuated peroxide-associated loss of viability and differentiation. Model: Mouse muscle-cell culture, 24-hour challenge experiments. Limitations: Does not identify a direct antioxidant reaction or an in-vivo effective dose. Evidence access: Primary full text Ionic Silicon Protects Oxidative Damage and Promotes Skeletal Muscle Cell Regeneration. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33419056/ · DOI 10.3390/ijms22020497
Complete structured claim and evidence
Silica nanoparticles increased inflammasome/pyroptosis-associated markers; MCC950 suppressed the response.
Silica nanoparticles, 2022 RAW-ASC preparation → Pyroptosis-associated response in mouse RAW-ASC cells source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Mouse RAW-ASC cells; LPS priming, 100 micrograms/mL silica, approximately 30 nm particles.
limitations
Do not assume all sizes, coatings or amorphous preparations behave identically.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
A nanoparticle preparation was examined separately from quartz.
primary_references
Characterization of Cathepsin B in Mediating Silica Nanoparticle-Induced Macrophage Pyroptosis via an NLRP3-Dependent Manner. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35966002/ · DOI 10.2147/JIR.S371536
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 504–510
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse RAW-ASC cells; LPS priming, 100 micrograms/mL silica, approximately 30 nm particles. · source_derived_draft · unverified_draft
## silica-nanoparticle-nlrp3 A nanoparticle preparation was examined separately from quartz. Silica nanoparticles increased inflammasome/pyroptosis-associated markers; MCC950 suppressed the response. Model: Mouse RAW-ASC cells; LPS priming, 100 micrograms/mL silica, approximately 30 nm particles. Limitations: Do not assume all sizes, coatings or amorphous preparations behave identically. Evidence access: Primary full text Characterization of Cathepsin B in Mediating Silica Nanoparticle-Induced Macrophage Pyroptosis via an NLRP3-Dependent Manner. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35966002/ · DOI 10.2147/JIR.S371536
Complete structured claim and evidence
Orthosilicic acid attenuated TNF-induced NF-kappaB activation in the osteoblast experimental program.
Orthosilicic acid / Si(OH)4 → NF-kappaB activation in the 2016 silicate osteoblast study source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human MSC/mouse preosteoblast study; exact species for each downstream assay unresolved in accessed abstract.
limitations
Do not assign all downstream experiments to human cells or infer an oral anti-inflammatory treatment.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
A regulatory-RNA response was linked to lower inflammatory signaling.
primary_references
Orthosilicic acid, Si(OH)4, stimulates osteoblast differentiation in vitro by upregulating miR-146a to antagonize NF-κB activation. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27163405/ · DOI 10.1016/j.actbio.2016.05.007
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 520–526
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human MSC/mouse preosteoblast study; exact species for each downstream assay unresolved in accessed abstract. · source_derived_draft · unverified_draft
## silica-nfkb-regulation A regulatory-RNA response was linked to lower inflammatory signaling. Orthosilicic acid attenuated TNF-induced NF-kappaB activation in the osteoblast experimental program. Model: Human MSC/mouse preosteoblast study; exact species for each downstream assay unresolved in accessed abstract. Limitations: Do not assign all downstream experiments to human cells or infer an oral anti-inflammatory treatment. Evidence access: Primary abstract Orthosilicic acid, Si(OH)4, stimulates osteoblast differentiation in vitro by upregulating miR-146a to antagonize NF-κB activation. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27163405/ · DOI 10.1016/j.actbio.2016.05.007
Complete structured claim and evidence
Nlrp3-deficient macrophages failed to mount the normal silica-induced caspase-1/IL-1 beta response.
Mouse NLRP3 → Caspase-1 activation after silica in mouse macrophages source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary full text
experimental_model
LPS-primed mouse macrophage genetic comparison.
limitations
Priming and activation are separate; dietary silicon is not the particle stimulus. Correction record: A 2026 author correction replaces an erroneously duplicated lower-left Fig. 8c micrograph with the retrieved original. This is a figure correction, not a scientific contradiction or retraction. https://www.nature.com/articles/s41590-026-02468-9
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
The sensor is a distinct necessary component in this model.
primary_references
Silica crystals and aluminum salts activate the NALP3 inflammasome through phagosomal destabilization. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18604214/ · DOI 10.1038/ni.1631
trigger_kind
machinery_impairment Imported condition classification; unverified.
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 440–446
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · LPS-primed mouse macrophage genetic comparison. · source_derived_draft · unverified_draft
## silica-nlrp3-loss The sensor is a distinct necessary component in this model. Nlrp3-deficient macrophages failed to mount the normal silica-induced caspase-1/IL-1 beta response. Model: LPS-primed mouse macrophage genetic comparison. Limitations: Priming and activation are separate; dietary silicon is not the particle stimulus. Correction record: A 2026 author correction replaces an erroneously duplicated lower-left Fig. 8c micrograph with the retrieved original. This is a figure correction, not a scientific contradiction or retraction. https://www.nature.com/articles/s41590-026-02468-9 Evidence access: Primary full text Silica crystals and aluminum salts activate the NALP3 inflammasome through phagosomal destabilization. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18604214/ · DOI 10.1038/ni.1631
Complete structured claim and evidence
Noggin pretreatment suppressed silicon-associated SMAD1/5 phosphorylation, RUNX2 and collagen expression.
Noggin-treated human osteoblast-like cultures → Collagen synthesis response to orthosilicic acid source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Human osteoblast-like cell pharmacological experiment.
limitations
Noggin is a BMP antagonist, not a uniquely selective proof of BMP2 mediation.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
Blocking BMP signaling weakened the response.
primary_references
Biological Silicon Stimulates Collagen Type 1 and Osteocalcin Synthesis in Human Osteoblast-Like Cells Through the BMP-2/Smad/RUNX2 Signaling Pathway. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27025722/ · DOI 10.1007/s12011-016-0686-3
trigger_kind
machinery_impairment Imported condition classification; unverified.
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 160–166
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human osteoblast-like cell pharmacological experiment. · source_derived_draft · unverified_draft
## silica-noggin-block Blocking BMP signaling weakened the response. Noggin pretreatment suppressed silicon-associated SMAD1/5 phosphorylation, RUNX2 and collagen expression. Model: Human osteoblast-like cell pharmacological experiment. Limitations: Noggin is a BMP antagonist, not a uniquely selective proof of BMP2 mediation. Evidence access: Primary abstract Biological Silicon Stimulates Collagen Type 1 and Osteocalcin Synthesis in Human Osteoblast-Like Cells Through the BMP-2/Smad/RUNX2 Signaling Pathway. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27025722/ · DOI 10.1007/s12011-016-0686-3
Complete structured claim and evidence
Cybb/gp91phox-deficient macrophages retained silica-triggered inflammasome responses.
Mouse CYBB / gp91phox → Mouse silica inflammasome response source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Mouse macrophage genetic comparison.
limitations
Does not exclude every ROS source or establish NADPH depletion. Correction record: A 2026 author correction replaces an erroneously duplicated lower-left Fig. 8c micrograph with the retrieved original. This is a figure correction, not a scientific contradiction or retraction. https://www.nature.com/articles/s41590-026-02468-9
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
The phagocyte NADPH oxidase burst was not obligatory in this model.
primary_references
Silica crystals and aluminum salts activate the NALP3 inflammasome through phagosomal destabilization. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18604214/ · DOI 10.1038/ni.1631
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 456–462
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse macrophage genetic comparison. · source_derived_draft · unverified_draft
## silica-nox2-null The phagocyte NADPH oxidase burst was not obligatory in this model. Cybb/gp91phox-deficient macrophages retained silica-triggered inflammasome responses. Model: Mouse macrophage genetic comparison. Limitations: Does not exclude every ROS source or establish NADPH depletion. Correction record: A 2026 author correction replaces an erroneously duplicated lower-left Fig. 8c micrograph with the retrieved original. This is a figure correction, not a scientific contradiction or retraction. https://www.nature.com/articles/s41590-026-02468-9 Evidence access: Primary full text Silica crystals and aluminum salts activate the NALP3 inflammasome through phagosomal destabilization. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18604214/ · DOI 10.1038/ni.1631
Complete structured claim and evidence
Oligomeric silica reduced aluminum tracer availability by 67% in the three-person comparison.
Oligomeric silicic acid → Aluminum(III) source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human aluminum-26 tracer study; 17 mg silica preparation as reported.
limitations
Very small study; does not establish treatment of aluminum toxicity.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
A less readily absorbed polymer can bind aluminum in the gut.
primary_references
Oligomeric but not monomeric silica prevents aluminum absorption in humans. · 2000 · https://pubmed.ncbi.nlm.nih.gov/10731501/ · DOI 10.1093/ajcn/71.4.944
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 88–94
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human aluminum-26 tracer study; 17 mg silica preparation as reported. · source_derived_draft · unverified_draft
## silica-oligomer-aluminum A less readily absorbed polymer can bind aluminum in the gut. Oligomeric silica reduced aluminum tracer availability by 67% in the three-person comparison. Model: Human aluminum-26 tracer study; 17 mg silica preparation as reported. Limitations: Very small study; does not establish treatment of aluminum toxicity. Evidence access: Primary abstract Oligomeric but not monomeric silica prevents aluminum absorption in humans. · 2000 · https://pubmed.ncbi.nlm.nih.gov/10731501/ · DOI 10.1093/ajcn/71.4.944
Complete structured claim and evidence
Median minimum uptake estimated from urine was 50.3% in eight volunteers receiving orthosilicic acid.
Orthosilicic acid / Si(OH)4 → Human gastrointestinal uptake of soluble silicon source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Water containing 27–55 mg Si/L; small human kinetic study.
limitations
Urinary recovery is a lower-bound estimate, not direct intracellular measurement.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
A substantial fraction of soluble silicon entered the body.
primary_references
Silicic acid: its gastrointestinal uptake and urinary excretion in man and effects on aluminium excretion. · 1999 · https://pubmed.ncbi.nlm.nih.gov/10612067/ · DOI 10.1016/s0162-0134(99)00126-9
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 64–70
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Water containing 27–55 mg Si/L; small human kinetic study. · source_derived_draft · unverified_draft
## silica-oral-uptake A substantial fraction of soluble silicon entered the body. Median minimum uptake estimated from urine was 50.3% in eight volunteers receiving orthosilicic acid. Model: Water containing 27–55 mg Si/L; small human kinetic study. Limitations: Urinary recovery is a lower-bound estimate, not direct intracellular measurement. Evidence access: Primary abstract Silicic acid: its gastrointestinal uptake and urinary excretion in man and effects on aluminium excretion. · 1999 · https://pubmed.ncbi.nlm.nih.gov/10612067/ · DOI 10.1016/s0162-0134(99)00126-9
Complete structured claim and evidence
At 1,700 micromolar orthosilicic acid, Saos-2 colony survival was about 20% below control, with reduced proliferation/adhesion.
Orthosilicic acid / Si(OH)4 → Human Saos-2 colony survival source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human osteoblast-like culture comparison, up to solubility limit.
limitations
Different concentration and endpoints from low-dose collagen studies; not a fabricated contradiction.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
Higher exposure was not uniformly beneficial.
primary_references
Divergent effects of orthosilicic acid and dimethylsilanediol on cell survival and adhesion in human osteoblast-like cells. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18755397/ · DOI 10.1016/j.jtemb.2008.02.001
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 200–206
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human osteoblast-like culture comparison, up to solubility limit. · source_derived_draft · unverified_draft
## silica-osa-high-exposure Higher exposure was not uniformly beneficial. At 1,700 micromolar orthosilicic acid, Saos-2 colony survival was about 20% below control, with reduced proliferation/adhesion. Model: Human osteoblast-like culture comparison, up to solubility limit. Limitations: Different concentration and endpoints from low-dose collagen studies; not a fabricated contradiction. Evidence access: Primary abstract Divergent effects of orthosilicic acid and dimethylsilanediol on cell survival and adhesion in human osteoblast-like cells. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18755397/ · DOI 10.1016/j.jtemb.2008.02.001
Complete structured claim and evidence
The silicon preparation lowered Tartrate-resistant acid phosphatase mRNA at 48 and 72 hours.
Silicon preparation containing 75% orthosilicic acid → Human Tartrate-resistant acid phosphatase source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Human RANKL-stimulated CD14+ cultures, 50 micrograms Si/mL.
limitations
Transcript abundance is not direct inhibition of the protein.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
A specific osteoclast marker changed during differentiation.
primary_references
Orthosilicic acid inhibits human osteoclast differentiation and bone resorption. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39405281/ · DOI 10.1371/journal.pone.0312169
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 232–238
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human RANKL-stimulated CD14+ cultures, 50 micrograms Si/mL. · source_derived_draft · unverified_draft
## silica-osteoclast-acp5 A specific osteoclast marker changed during differentiation. The silicon preparation lowered Tartrate-resistant acid phosphatase mRNA at 48 and 72 hours. Model: Human RANKL-stimulated CD14+ cultures, 50 micrograms Si/mL. Limitations: Transcript abundance is not direct inhibition of the protein. Evidence access: Primary full text Orthosilicic acid inhibits human osteoclast differentiation and bone resorption. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39405281/ · DOI 10.1371/journal.pone.0312169
Complete structured claim and evidence
AQP9 mRNA increased significantly at 72 hours during silicon exposure.
Silicon preparation containing 75% orthosilicic acid → Human aquaporin 9 / AQP9 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Human CD14+ osteoclast cultures.
limitations
No AQP9 loss-of-function test demonstrated that it mediated the resorption effect.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
Transporter expression changed even while differentiation markers fell.
primary_references
Orthosilicic acid inhibits human osteoclast differentiation and bone resorption. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39405281/ · DOI 10.1371/journal.pone.0312169
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 256–262
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human CD14+ osteoclast cultures. · source_derived_draft · unverified_draft
## silica-osteoclast-aqp9 Transporter expression changed even while differentiation markers fell. AQP9 mRNA increased significantly at 72 hours during silicon exposure. Model: Human CD14+ osteoclast cultures. Limitations: No AQP9 loss-of-function test demonstrated that it mediated the resorption effect. Evidence access: Primary full text Orthosilicic acid inhibits human osteoclast differentiation and bone resorption. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39405281/ · DOI 10.1371/journal.pone.0312169
Complete structured claim and evidence
The silicon preparation lowered Calcitonin receptor mRNA at 48 hours.
Silicon preparation containing 75% orthosilicic acid → Human Calcitonin receptor source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Human RANKL-stimulated CD14+ cultures, 50 micrograms Si/mL.
limitations
Transcript abundance is not direct inhibition of the protein.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
A specific osteoclast marker changed during differentiation.
primary_references
Orthosilicic acid inhibits human osteoclast differentiation and bone resorption. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39405281/ · DOI 10.1371/journal.pone.0312169
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 240–246
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human RANKL-stimulated CD14+ cultures, 50 micrograms Si/mL. · source_derived_draft · unverified_draft
## silica-osteoclast-calcr A specific osteoclast marker changed during differentiation. The silicon preparation lowered Calcitonin receptor mRNA at 48 hours. Model: Human RANKL-stimulated CD14+ cultures, 50 micrograms Si/mL. Limitations: Transcript abundance is not direct inhibition of the protein. Evidence access: Primary full text Orthosilicic acid inhibits human osteoclast differentiation and bone resorption. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39405281/ · DOI 10.1371/journal.pone.0312169
Complete structured claim and evidence
The silicon preparation lowered Cathepsin K mRNA at 48 and 72 hours.
Silicon preparation containing 75% orthosilicic acid → Human Cathepsin K source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Human RANKL-stimulated CD14+ cultures, 50 micrograms Si/mL.
limitations
Transcript abundance is not direct inhibition of the protein.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
A specific osteoclast marker changed during differentiation.
primary_references
Orthosilicic acid inhibits human osteoclast differentiation and bone resorption. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39405281/ · DOI 10.1371/journal.pone.0312169
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 224–230
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human RANKL-stimulated CD14+ cultures, 50 micrograms Si/mL. · source_derived_draft · unverified_draft
## silica-osteoclast-ctsk A specific osteoclast marker changed during differentiation. The silicon preparation lowered Cathepsin K mRNA at 48 and 72 hours. Model: Human RANKL-stimulated CD14+ cultures, 50 micrograms Si/mL. Limitations: Transcript abundance is not direct inhibition of the protein. Evidence access: Primary full text Orthosilicic acid inhibits human osteoclast differentiation and bone resorption. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39405281/ · DOI 10.1371/journal.pone.0312169
Complete structured claim and evidence
The silicon preparation lowered DC-STAMP mRNA at 48 and 96 hours.
Silicon preparation containing 75% orthosilicic acid → Human DC-STAMP source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Human RANKL-stimulated CD14+ cultures, 50 micrograms Si/mL.
limitations
Transcript abundance is not direct inhibition of the protein.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
A specific osteoclast marker changed during differentiation.
primary_references
Orthosilicic acid inhibits human osteoclast differentiation and bone resorption. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39405281/ · DOI 10.1371/journal.pone.0312169
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 248–254
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human RANKL-stimulated CD14+ cultures, 50 micrograms Si/mL. · source_derived_draft · unverified_draft
## silica-osteoclast-dcstamp A specific osteoclast marker changed during differentiation. The silicon preparation lowered DC-STAMP mRNA at 48 and 96 hours. Model: Human RANKL-stimulated CD14+ cultures, 50 micrograms Si/mL. Limitations: Transcript abundance is not direct inhibition of the protein. Evidence access: Primary full text Orthosilicic acid inhibits human osteoclast differentiation and bone resorption. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39405281/ · DOI 10.1371/journal.pone.0312169
Complete structured claim and evidence
The 75%-OSA silicon preparation reduced RANKL-stimulated TRAP-positive multinucleated human osteoclasts.
Silicon preparation containing 75% orthosilicic acid → Human osteoclast differentiation under silicon exposure source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Human CD14+ monocytes, M-CSF and recombinant mouse RANKL; 50 micrograms Si/mL.
limitations
About 1.8 mM total Si, not a normal plasma exposure or chemically pure OSA.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
Fewer bone-resorbing cells formed under these culture conditions.
primary_references
Orthosilicic acid inhibits human osteoclast differentiation and bone resorption. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39405281/ · DOI 10.1371/journal.pone.0312169
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 216–222
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human CD14+ monocytes, M-CSF and recombinant mouse RANKL; 50 micrograms Si/mL. · source_derived_draft · unverified_draft
## silica-osteoclast-differentiation Fewer bone-resorbing cells formed under these culture conditions. The 75%-OSA silicon preparation reduced RANKL-stimulated TRAP-positive multinucleated human osteoclasts. Model: Human CD14+ monocytes, M-CSF and recombinant mouse RANKL; 50 micrograms Si/mL. Limitations: About 1.8 mM total Si, not a normal plasma exposure or chemically pure OSA. Evidence access: Primary full text Orthosilicic acid inhibits human osteoclast differentiation and bone resorption. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39405281/ · DOI 10.1371/journal.pone.0312169
Complete structured claim and evidence
Silicon treatment reduced resorption pits and released type I collagen fragments on bone slices.
Silicon preparation containing 75% orthosilicic acid → Human osteoclast bone resorption source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Human osteoclast bone-disc assays; 50 micrograms Si/mL.
limitations
Not demonstrated clinical fracture prevention.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
The study measured matrix breakdown as well as cell markers.
primary_references
Orthosilicic acid inhibits human osteoclast differentiation and bone resorption. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39405281/ · DOI 10.1371/journal.pone.0312169
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 264–270
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human osteoclast bone-disc assays; 50 micrograms Si/mL. · source_derived_draft · unverified_draft
## silica-osteoclast-resorption The study measured matrix breakdown as well as cell markers. Silicon treatment reduced resorption pits and released type I collagen fragments on bone slices. Model: Human osteoclast bone-disc assays; 50 micrograms Si/mL. Limitations: Not demonstrated clinical fracture prevention. Evidence access: Primary full text Orthosilicic acid inhibits human osteoclast differentiation and bone resorption. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39405281/ · DOI 10.1371/journal.pone.0312169
Complete structured claim and evidence
NFS-rich silica strongly adsorbed zwitterionic phospholipid assemblies and disrupted their order more than negatively charged liposomes.
Nearly free surface silanols on silica particles → Phosphatidylcholine source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Model membranes and computational recognition analysis.
limitations
Membrane interaction is not evidence that choline intake increases silica injury or protects against it.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
The phosphocholine headgroup creates a molecular link to membrane composition.
primary_references
Molecular recognition between membrane epitopes and nearly free surface silanols explains silica membranolytic activity. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35738078/ · DOI 10.1016/j.colsurfb.2022.112625
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 400–406
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Model membranes and computational recognition analysis. · source_derived_draft · unverified_draft
## silica-phosphocholine-recognition The phosphocholine headgroup creates a molecular link to membrane composition. NFS-rich silica strongly adsorbed zwitterionic phospholipid assemblies and disrupted their order more than negatively charged liposomes. Model: Model membranes and computational recognition analysis. Limitations: Membrane interaction is not evidence that choline intake increases silica injury or protects against it. Evidence access: Primary full text Molecular recognition between membrane epitopes and nearly free surface silanols explains silica membranolytic activity. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35738078/ · DOI 10.1016/j.colsurfb.2022.112625
Complete structured claim and evidence
Orthosilicic acid increased PI3K, phosphorylated Akt and mTOR together with osteogenic markers.
Orthosilicic acid / Si(OH)4 → Human mechanistic target of rapamycin kinase / MTOR source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human osteoblast-like cell study.
limitations
No direct binding target or dietary requirement is established.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
A growth-related pathway accompanied matrix production.
primary_references
Orthosilicic Acid Accelerates Bone Formation in Human Osteoblast-Like Cells Through the PI3K-Akt-mTOR Pathway. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30421162/ · DOI 10.1007/s12011-018-1574-9
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 168–174
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human osteoblast-like cell study. · source_derived_draft · unverified_draft
## silica-pi3k-mtor A growth-related pathway accompanied matrix production. Orthosilicic acid increased PI3K, phosphorylated Akt and mTOR together with osteogenic markers. Model: Human osteoblast-like cell study. Limitations: No direct binding target or dietary requirement is established. Evidence access: Primary abstract Orthosilicic Acid Accelerates Bone Formation in Human Osteoblast-Like Cells Through the PI3K-Akt-mTOR Pathway. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30421162/ · DOI 10.1007/s12011-018-1574-9
Complete structured claim and evidence
High extracellular potassium blocked silica-induced caspase-1 processing and IL-1 beta release, including during low-dose uptake blockade.
Potassium ion → Mouse IL-1 beta source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Mouse macrophages; 130 mM KCl experimental condition.
limitations
Not a potassium supplement treatment; no specific channel identity was established.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
The potassium gradient gates this inflammatory response.
primary_references
Activation of NLRP3 inflammasome by crystalline structures via cell surface contact. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25445147/ · DOI 10.1038/srep07281
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 480–486
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse macrophages; 130 mM KCl experimental condition. · source_derived_draft · unverified_draft
## silica-potassium-gate The potassium gradient gates this inflammatory response. High extracellular potassium blocked silica-induced caspase-1 processing and IL-1 beta release, including during low-dose uptake blockade. Model: Mouse macrophages; 130 mM KCl experimental condition. Limitations: Not a potassium supplement treatment; no specific channel identity was established. Evidence access: Primary full text Activation of NLRP3 inflammasome by crystalline structures via cell surface contact. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25445147/ · DOI 10.1038/srep07281
Complete structured claim and evidence
Low-silicon diets reduced hydroxyproline in rat bone and wound sponges relative to supplemented diets.
Low-silicon experimental rat diet → Hydroxyproline in rat bone and implanted wound sponges source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Basal diets 2 or 2.6 micrograms Si/g; comparison added 10 micrograms Si/g as sodium metasilicate.
limitations
No validated human deficiency syndrome or blood threshold follows.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
An animal low-intake model altered collagen-related endpoints.
primary_references
Silicon deprivation decreases collagen formation in wounds and bone, and ornithine transaminase enzyme activity in liver. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12462748/ · DOI 10.1385/bter:89:3:251
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 352–358
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Basal diets 2 or 2.6 micrograms Si/g; comparison added 10 micrograms Si/g as sodium metasilicate. · source_derived_draft · unverified_draft
## silica-rat-deprivation-collagen An animal low-intake model altered collagen-related endpoints. Low-silicon diets reduced hydroxyproline in rat bone and wound sponges relative to supplemented diets. Model: Basal diets 2 or 2.6 micrograms Si/g; comparison added 10 micrograms Si/g as sodium metasilicate. Limitations: No validated human deficiency syndrome or blood threshold follows. Evidence access: Primary abstract Silicon deprivation decreases collagen formation in wounds and bone, and ornithine transaminase enzyme activity in liver. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12462748/ · DOI 10.1385/bter:89:3:251
Complete structured claim and evidence
Rat liver ornithine aminotransferase activity decreased with silicon deprivation.
Low-silicon experimental rat diet → Rat ornithine aminotransferase / OAT source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Rat dietary comparison; liver enzyme assay.
limitations
Activity change does not prove silicon is an OAT cofactor or a direct link to vitamin B6 depletion.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
A proline-related metabolic enzyme changed alongside collagen endpoints.
primary_references
Silicon deprivation decreases collagen formation in wounds and bone, and ornithine transaminase enzyme activity in liver. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12462748/ · DOI 10.1385/bter:89:3:251
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 360–366
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat dietary comparison; liver enzyme assay. · source_derived_draft · unverified_draft
## silica-rat-oat A proline-related metabolic enzyme changed alongside collagen endpoints. Rat liver ornithine aminotransferase activity decreased with silicon deprivation. Model: Rat dietary comparison; liver enzyme assay. Limitations: Activity change does not prove silicon is an OAT cofactor or a direct link to vitamin B6 depletion. Evidence access: Primary abstract Silicon deprivation decreases collagen formation in wounds and bone, and ornithine transaminase enzyme activity in liver. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12462748/ · DOI 10.1385/bter:89:3:251
Complete structured claim and evidence
Reported silicon renal clearance was 82–96 mL/min and correlated with creatinine clearance.
Orthosilicic acid / Si(OH)4 → Renal clearance of silicon in humans source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Healthy volunteer kinetics.
limitations
No universal tissue sufficiency threshold follows from serum or urine silicon.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
Kidney function affects measured silicon handling.
primary_references
Silicic acid: its gastrointestinal uptake and urinary excretion in man and effects on aluminium excretion. · 1999 · https://pubmed.ncbi.nlm.nih.gov/10612067/ · DOI 10.1016/s0162-0134(99)00126-9
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 72–78
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Healthy volunteer kinetics. · source_derived_draft · unverified_draft
## silica-renal-clearance Kidney function affects measured silicon handling. Reported silicon renal clearance was 82–96 mL/min and correlated with creatinine clearance. Model: Healthy volunteer kinetics. Limitations: No universal tissue sufficiency threshold follows from serum or urine silicon. Evidence access: Primary abstract Silicic acid: its gastrointestinal uptake and urinary excretion in man and effects on aluminium excretion. · 1999 · https://pubmed.ncbi.nlm.nih.gov/10612067/ · DOI 10.1016/s0162-0134(99)00126-9
Complete structured claim and evidence
Particle surface treatments linked nearly free silanols to membranolysis and inflammatory activity.
Nearly free surface silanols on silica particles → Membrane disruption by silica particles source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Characterized quartz/amorphous particles, membrane assays, macrophages and rat exposure program.
limitations
Surface motif is not a dissolved nutrient species; no oral-dose inference.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
Surface chemistry helps explain why silica preparations differ.
primary_references
Nearly free surface silanols are the critical molecular moieties that initiate the toxicity of silica particles. · 2020 · https://pubmed.ncbi.nlm.nih.gov/33097669/ · DOI 10.1073/pnas.2008006117
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 392–398
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Characterized quartz/amorphous particles, membrane assays, macrophages and rat exposure program. · source_derived_draft · unverified_draft
## silica-silanol-membrane Surface chemistry helps explain why silica preparations differ. Particle surface treatments linked nearly free silanols to membranolysis and inflammatory activity. Model: Characterized quartz/amorphous particles, membrane assays, macrophages and rat exposure program. Limitations: Surface motif is not a dissolved nutrient species; no oral-dose inference. Evidence access: Primary full text Nearly free surface silanols are the critical molecular moieties that initiate the toxicity of silica particles. · 2020 · https://pubmed.ncbi.nlm.nih.gov/33097669/ · DOI 10.1073/pnas.2008006117
Complete structured claim and evidence
Orthosilicic acid increased phosphorylated SMAD1/5 and RUNX2 expression alongside osteogenic markers.
Orthosilicic acid / Si(OH)4 → Human SMAD1/SMAD5 signaling proteins source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human osteoblast-like cell lines, 10 micromolar exposure.
limitations
Marker regulation does not prove each edge by direct binding.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
The response extended to downstream bone-development regulators.
primary_references
Biological Silicon Stimulates Collagen Type 1 and Osteocalcin Synthesis in Human Osteoblast-Like Cells Through the BMP-2/Smad/RUNX2 Signaling Pathway. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27025722/ · DOI 10.1007/s12011-016-0686-3
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 152–158
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human osteoblast-like cell lines, 10 micromolar exposure. · source_derived_draft · unverified_draft
## silica-smad-runx2 The response extended to downstream bone-development regulators. Orthosilicic acid increased phosphorylated SMAD1/5 and RUNX2 expression alongside osteogenic markers. Model: Human osteoblast-like cell lines, 10 micromolar exposure. Limitations: Marker regulation does not prove each edge by direct binding. Evidence access: Primary abstract Biological Silicon Stimulates Collagen Type 1 and Osteocalcin Synthesis in Human Osteoblast-Like Cells Through the BMP-2/Smad/RUNX2 Signaling Pathway. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27025722/ · DOI 10.1007/s12011-016-0686-3
Complete structured claim and evidence
Cytochalasin D blocked silica uptake and IL-1 beta release, supporting a phagocytosis-dependent interpretation.
Cytochalasin-D uptake blockade in the 2008 silica study → Mouse IL-1 beta source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary full text
experimental_model
Mouse macrophages; related human PBMC result separately reported in the paper.
limitations
Inhibitor dose and non-uptake effects require comparison with later low-dose experiments. Correction record: A 2026 author correction replaces an erroneously duplicated lower-left Fig. 8c micrograph with the retrieved original. This is a figure correction, not a scientific contradiction or retraction. https://www.nature.com/articles/s41590-026-02468-9
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
Blocking engulfment also blocked inflammatory output in this experiment.
primary_references
Silica crystals and aluminum salts activate the NALP3 inflammasome through phagosomal destabilization. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18604214/ · DOI 10.1038/ni.1631
trigger_kind
machinery_impairment Imported condition classification; unverified.
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 432–438
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse macrophages; related human PBMC result separately reported in the paper. · source_derived_draft · unverified_draft
## silica-uptake-block-2008 Blocking engulfment also blocked inflammatory output in this experiment. Cytochalasin D blocked silica uptake and IL-1 beta release, supporting a phagocytosis-dependent interpretation. Model: Mouse macrophages; related human PBMC result separately reported in the paper. Limitations: Inhibitor dose and non-uptake effects require comparison with later low-dose experiments. Correction record: A 2026 author correction replaces an erroneously duplicated lower-left Fig. 8c micrograph with the retrieved original. This is a figure correction, not a scientific contradiction or retraction. https://www.nature.com/articles/s41590-026-02468-9 Evidence access: Primary full text Silica crystals and aluminum salts activate the NALP3 inflammasome through phagosomal destabilization. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18604214/ · DOI 10.1038/ni.1631
Complete structured claim and evidence
Low-dose cytochalasin D blocked silica engulfment while preserving caspase-1 processing and IL-1 beta release.
Low-dose cytochalasin D in the 2014 silica study → Mouse IL-1 beta source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Mouse bone-marrow macrophages; 0.25–0.5 micromolar cytochalasin D.
limitations
Immobilized epoxy-crystal experiments used MSU, not silica; do not transfer that detail between materials.
nutrient_topic
Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
plain_language
Surface-associated crystals could still trigger a response when uptake was blocked.
primary_references
Activation of NLRP3 inflammasome by crystalline structures via cell surface contact. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25445147/ · DOI 10.1038/srep07281
Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 464–470
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse bone-marrow macrophages; 0.25–0.5 micromolar cytochalasin D. · source_derived_draft · unverified_draft
## silica-uptake-block-2014 Surface-associated crystals could still trigger a response when uptake was blocked. Low-dose cytochalasin D blocked silica engulfment while preserving caspase-1 processing and IL-1 beta release. Model: Mouse bone-marrow macrophages; 0.25–0.5 micromolar cytochalasin D. Limitations: Immobilized epoxy-crystal experiments used MSU, not silica; do not transfer that detail between materials. Evidence access: Primary full text Activation of NLRP3 inflammasome by crystalline structures via cell surface contact. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25445147/ · DOI 10.1038/srep07281
Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

Evidence, AI assistance and curation standards

Silica and soluble silicon

How nutrients influence it

Other things that act on it

How nutrients reach it in more than one step

What it does

Where it participates (unsigned role)

Orthosilicic acid in water did not significantly increase endogenous aluminum excretion over 32 hours in five volunteers.

Beer-derived monosilicic acid ingestion was accompanied by increased urinary aluminum in this study.

Combined AQP3/AQP7/AQP9/AQP10 RNA interference reduced silicon efflux from preloaded HEK-293 cells.

Expression of human AQP10 increased silicon transport in the tested oocyte and HEK-293 systems.

Expression of human AQP3 increased silicon transport in the tested oocyte and HEK-293 systems.

Expression of human AQP7 increased silicon transport in the tested oocyte and HEK-293 systems.

Phloretin increased AQP9-mediated silicon influx under the tested hypoosmolar conditions while inhibiting water transport.

Expression of human AQP9 increased silicon transport in the tested oocyte and HEK-293 systems.

Ten micromolar orthosilicic acid increased BMP2 expression in human osteoblast-like cells.

CA-074-Me reduced silica-triggered IL-1 beta release, supporting a cathepsin-sensitive step.

Cathepsin-B-deficient macrophages retained crystal-induced IL-1 beta release in this study.

Silicon-deprived chicks showed abnormal epiphyseal cartilage and lower tibial hexosamine/collagen measures.

U18666A-induced cholesterol accumulation reduced silica-induced inflammasome activation in mouse alveolar macrophages.

Orthosilicic acid at 10–20 micromolar increased type I collagen synthesis in human osteoblast-like cultures.

Type I collagen mRNA did not increase despite greater collagen synthesis in treated MG-63 cells.

Thirty micromolar OSA improved HUVEC proliferation, migration and tube formation under high glucose.

OSA improved skin-wound healing in db/db mice, with PI3K/Akt/mTOR involvement reported.

Dimethylsilanediol had no discernible survival effect up to 50 micromolar and increased survival at higher tested doses.

Silicon-treated HUVECs increased catalase mRNA under the reported normal and peroxide conditions.

The 0.5 mM silicon preparation increased HIF1A expression in HUVECs with or without the tested peroxide challenge.

The 0.5 mM silicon preparation increased VEGFR2 / KDR expression in HUVECs with or without the tested peroxide challenge.

The 0.5 mM silicon preparation increased VEGFA expression in HUVECs with or without the tested peroxide challenge.

Silicon-treated HUVECs increased NOS3 mRNA under the reported normal and peroxide conditions.

Silicon-treated HUVECs increased SOD1 mRNA under the reported normal and peroxide conditions.

A 0.5 mM silicon preparation improved HUVEC viability during hydrogen-peroxide exposure.

Urinary recovery was approximately 43% for orthosilicic acid, 17% for choline-stabilized acid and 1% for colloidal silica in this comparison.

Lumbar spine BMD did not significantly change; a femoral-neck signal arose in a post-hoc subgroup.

Human MARCO expression in CHO cells supported silica binding and apoptosis.

PINP differed from placebo at 12 months in the 6- and 12-mg Si groups without a clear dose response.

Prolyl hydroxylase inhibitors abolished the orthosilicic-acid-associated collagen increase.

Leupeptin reduced the measured cathepsin-B signal without preventing the nanoparticle-associated pyroptosis response.

LY294002 reduced pathway signals and osteogenic markers during orthosilicic acid treatment.

Phagocytosed silica caused lysosomal swelling and leakage in mouse macrophages.

MARCO-null alveolar macrophages showed greater lysosomal leakage and IL-1 beta/caspase-1 responses despite lower silica uptake.

MARCO loss or antibody blockade prevented silica uptake and cytotoxicity in C57BL/6 alveolar macrophages.

Silicon-releasing microcarriers increased HIF1A expression and stabilization, attributed to reduced PHD2 activity in HUVECs.

Microcarriers releasing silicon and loaded VEGF increased endothelial migration and tubular networking.

Orthosilicic acid increased miR-146a during later osteogenic differentiation of human mesenchymal stromal cells.

The monomeric preparation did not significantly reduce aluminum availability in the same study.

Anti-miR-146a suppressed differentiation in MC3T3 preosteoblasts in the silicate study.

A 0.1 mM silicon preparation increased C2C12 viability, migration and myotube formation.

Silicon preparations at 0.1–2 mM attenuated peroxide-associated loss of viability and differentiation.

Silica nanoparticles increased inflammasome/pyroptosis-associated markers; MCC950 suppressed the response.

Orthosilicic acid attenuated TNF-induced NF-kappaB activation in the osteoblast experimental program.

Nlrp3-deficient macrophages failed to mount the normal silica-induced caspase-1/IL-1 beta response.

Noggin pretreatment suppressed silicon-associated SMAD1/5 phosphorylation, RUNX2 and collagen expression.

Cybb/gp91phox-deficient macrophages retained silica-triggered inflammasome responses.

Oligomeric silica reduced aluminum tracer availability by 67% in the three-person comparison.

Median minimum uptake estimated from urine was 50.3% in eight volunteers receiving orthosilicic acid.

At 1,700 micromolar orthosilicic acid, Saos-2 colony survival was about 20% below control, with reduced proliferation/adhesion.

The silicon preparation lowered Tartrate-resistant acid phosphatase mRNA at 48 and 72 hours.

AQP9 mRNA increased significantly at 72 hours during silicon exposure.

The silicon preparation lowered Calcitonin receptor mRNA at 48 hours.

The silicon preparation lowered Cathepsin K mRNA at 48 and 72 hours.

The silicon preparation lowered DC-STAMP mRNA at 48 and 96 hours.

The 75%-OSA silicon preparation reduced RANKL-stimulated TRAP-positive multinucleated human osteoclasts.

Silicon treatment reduced resorption pits and released type I collagen fragments on bone slices.

NFS-rich silica strongly adsorbed zwitterionic phospholipid assemblies and disrupted their order more than negatively charged liposomes.

Orthosilicic acid increased PI3K, phosphorylated Akt and mTOR together with osteogenic markers.

High extracellular potassium blocked silica-induced caspase-1 processing and IL-1 beta release, including during low-dose uptake blockade.

Low-silicon diets reduced hydroxyproline in rat bone and wound sponges relative to supplemented diets.

Rat liver ornithine aminotransferase activity decreased with silicon deprivation.

Reported silicon renal clearance was 82–96 mL/min and correlated with creatinine clearance.

Particle surface treatments linked nearly free silanols to membranolysis and inflammatory activity.

Orthosilicic acid increased phosphorylated SMAD1/5 and RUNX2 expression alongside osteogenic markers.

Cytochalasin D blocked silica uptake and IL-1 beta release, supporting a phagocytosis-dependent interpretation.

Low-dose cytochalasin D blocked silica engulfment while preserving caspase-1 processing and IL-1 beta release.

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