Component

Farnesyl diphosphate / FPP

Fifteen-carbon isoprenoid; the arm that did not reverse the endothelial response.

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

Where it participates (unsigned role)

  1. Geranylgeranyl diphosphate reversed the statin-induced rise in endothelial nitric oxide synthase, while farnesyl diphosphate and low-density lipoprotein did not.

    Geranylgeranyl diphosphate / GGPP → Human endothelial nitric oxide synthase / eNOS / NOS3 source_derived_draftungraded
    Experimental context and source evidence
    duration
    Not stated here
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    Human endothelial cells
    exposure
    Geranylgeranyl diphosphate 1 to 10 micromolar, farnesyl diphosphate 5 to 10 micromolar, L-mevalonate 200 micromolar or LDL 1 mg/ml added with mevastatin
    limitations
    This identifies which isoprenoid carries the effect; it does not establish that geranylgeranyl diphosphate is limiting at ordinary statin doses in a person.
    organism
    Human endothelial cells
    plain_language
    Geranylgeranyl diphosphate reversed the statin-induced rise in endothelial nitric oxide synthase, while farnesyl diphosphate and low-density lipoprotein did not.
    primary_references
    Post-transcriptional regulation of endothelial nitric oxide synthase mRNA stability by Rho GTPase. (1998). https://pubmed.ncbi.nlm.nih.gov/9727051/ DOI: 10.1074/jbc.273.37.24266
    route
    In vitro
    tissue
    Endothelial nitric oxide synthase expression and Rho membrane translocation

    Atorvastatin: mechanism of action from target occupancy to isoprenoids, transport, muscle and metabolism (2026-09-22) · lines 67–76

    Original AI-assisted curation of twelve primary studies resolved by PubMed title search and cross-checked against live PubMed metadata. Findings obtained with mevastatin, simvastatin or the statin class are recorded against those subjects. Study-specific citations, doses, negative findings and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft

    ## ggpp-reverses-the-nos-response Geranylgeranyl diphosphate reversed the statin-induced rise in endothelial nitric oxide synthase, while farnesyl diphosphate and low-density lipoprotein did not. Model/species: Human endothelial cells Tissue/system: Endothelial nitric oxide synthase expression and Rho membrane translocation Exposure: Geranylgeranyl diphosphate 1 to 10 micromolar, farnesyl diphosphate 5 to 10 micromolar, L-mevalonate 200 micromolar or LDL 1 mg/ml added with mevastatin Route: In vitro Duration: Not stated here Limits: This identifies which isoprenoid carries the effect; it does not establish that geranylgeranyl diphosphate is limiting at ordinary statin doses in a person. Primary reference: Post-transcriptional regulation of endothelial nitric oxide synthase mRNA stability by Rho GTPase. (1998). https://pubmed.ncbi.nlm.nih.gov/9727051/ DOI: 10.1074/jbc.273.37.24266 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  2. The mevalonate pathway produces isoprenoids required for functions ranging from cholesterol synthesis to growth control, under feedback regulation that also governs low-density-lipoprotein receptors.

    Mevalonate → Geranylgeranyl diphosphate / GGPP source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    Review of mammalian mevalonate-pathway regulation
    exposure
    Not applicable
    limitations
    A review of regulatory architecture, not a measurement of any one statin's effect on any one isoprenoid pool.
    organism
    Review of mammalian mevalonate-pathway regulation
    plain_language
    The mevalonate pathway produces isoprenoids required for functions ranging from cholesterol synthesis to growth control, under feedback regulation that also governs low-density-lipoprotein receptors.
    primary_references
    Regulation of the mevalonate pathway. (1990). https://pubmed.ncbi.nlm.nih.gov/1967820/ DOI: 10.1038/343425a0
    route
    Not applicable
    tissue
    Isoprenoid and sterol end-products

    Atorvastatin: mechanism of action from target occupancy to isoprenoids, transport, muscle and metabolism (2026-09-22) · lines 24–32

    Original AI-assisted curation of twelve primary studies resolved by PubMed title search and cross-checked against live PubMed metadata. Findings obtained with mevastatin, simvastatin or the statin class are recorded against those subjects. Study-specific citations, doses, negative findings and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft

    ## mevalonate-supplies-isoprenoids The mevalonate pathway produces isoprenoids required for functions ranging from cholesterol synthesis to growth control, under feedback regulation that also governs low-density-lipoprotein receptors. Model/species: Review of mammalian mevalonate-pathway regulation Tissue/system: Isoprenoid and sterol end-products Exposure: Not applicable Route: Not applicable Limits: A review of regulatory architecture, not a measurement of any one statin's effect on any one isoprenoid pool. Primary reference: Regulation of the mevalonate pathway. (1990). https://pubmed.ncbi.nlm.nih.gov/1967820/ DOI: 10.1038/343425a0 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  3. Mevastatin inhibited Rho membrane translocation by about 60 percent and Rho GTP-binding activity by about 78 percent, both reversed by geranylgeranyl diphosphate but not by farnesyl diphosphate.

    Mevastatin → Rho membrane translocation and GTP binding source_derived_draftungraded
    Experimental context and source evidence
    duration
    Not stated here
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    Human endothelial cells
    exposure
    Mevastatin with or without geranylgeranyl diphosphate or farnesyl diphosphate
    limitations
    Measured for Rho as a group by immunoblot and GTP-gamma-S binding, not resolved to individual Rho family members.
    organism
    Human endothelial cells
    plain_language
    Mevastatin inhibited Rho membrane translocation by about 60 percent and Rho GTP-binding activity by about 78 percent, both reversed by geranylgeranyl diphosphate but not by farnesyl diphosphate.
    primary_references
    Post-transcriptional regulation of endothelial nitric oxide synthase mRNA stability by Rho GTPase. (1998). https://pubmed.ncbi.nlm.nih.gov/9727051/ DOI: 10.1074/jbc.273.37.24266
    route
    In vitro
    tissue
    Rho GTPase membrane localisation and nucleotide binding

    Atorvastatin: mechanism of action from target occupancy to isoprenoids, transport, muscle and metabolism (2026-09-22) · lines 78–87

    Original AI-assisted curation of twelve primary studies resolved by PubMed title search and cross-checked against live PubMed metadata. Findings obtained with mevastatin, simvastatin or the statin class are recorded against those subjects. Study-specific citations, doses, negative findings and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft

    ## statin-inhibits-rho-membrane-translocation Mevastatin inhibited Rho membrane translocation by about 60 percent and Rho GTP-binding activity by about 78 percent, both reversed by geranylgeranyl diphosphate but not by farnesyl diphosphate. Model/species: Human endothelial cells Tissue/system: Rho GTPase membrane localisation and nucleotide binding Exposure: Mevastatin with or without geranylgeranyl diphosphate or farnesyl diphosphate Route: In vitro Duration: Not stated here Limits: Measured for Rho as a group by immunoblot and GTP-gamma-S binding, not resolved to individual Rho family members. Primary reference: Post-transcriptional regulation of endothelial nitric oxide synthase mRNA stability by Rho GTPase. (1998). https://pubmed.ncbi.nlm.nih.gov/9727051/ DOI: 10.1074/jbc.273.37.24266 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    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