Component

Collagen synthesis response to orthosilicic acid

Context-specific entity; species, compartment and exposure are stated on each claim.

3 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.

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. 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

  2. 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

  3. 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

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