Component
Human type I collagen
Context-specific entity; species, compartment and exposure are stated on each claim.
7 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What acts on it
Orthosilicic acid at 10–20 micromolar increased type I collagen synthesis in human osteoblast-like cultures.
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
Where it participates (unsigned role)
Type I collagen mRNA did not increase despite greater collagen synthesis in treated MG-63 cells.
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 evidenceProlyl hydroxylase inhibitors abolished the orthosilicic-acid-associated collagen increase.
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 evidenceNoggin pretreatment suppressed silicon-associated SMAD1/5 phosphorylation, RUNX2 and collagen expression.
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 evidenceSilicon treatment reduced resorption pits and released type I collagen fragments on bone slices.
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 evidenceOrthosilicic acid increased PI3K, phosphorylated Akt and mTOR together with osteogenic markers.
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 evidenceOrthosilicic acid increased phosphorylated SMAD1/5 and RUNX2 expression alongside osteogenic markers.
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
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.