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.

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

What acts on it

  1. 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

Where it participates (unsigned role)

  1. 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 evidence
  2. Prolyl 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 evidence
  3. Noggin 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 evidence
  4. Silicon 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 evidence
  5. Orthosilicic 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 evidence
  6. Orthosilicic 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

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