Component

SLCO1B1 rs4363657 variant

Noncoding variant within SLCO1B1 carrying the genome-wide myopathy signal.

1 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 it acts on

  1. A genome-wide association study found a single strong association of statin myopathy with the rs4363657 variant within SLCO1B1, which encodes the hepatic uptake transporter OATP1B1.

    Experimental context and source evidence
    duration
    Trial duration, not stated here
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    85 subjects with definite or incipient myopathy and 90 controls, replicated in a separate trial
    exposure
    Simvastatin 80 mg daily, replication at simvastatin 40 mg daily
    limitations
    The statin was simvastatin, not atorvastatin, and the association is with a noncoding variant rather than a demonstrated change in transporter function in these subjects.
    organism
    85 subjects with definite or incipient myopathy and 90 controls, replicated in a separate trial
    plain_language
    A genome-wide association study found a single strong association of statin myopathy with the rs4363657 variant within SLCO1B1, which encodes the hepatic uptake transporter OATP1B1.
    primary_references
    SLCO1B1 variants and statin-induced myopathy--a genomewide study. (2008). https://pubmed.ncbi.nlm.nih.gov/18650507/ DOI: 10.1056/NEJMoa0801936
    route
    Oral
    tissue
    Hepatic statin uptake and skeletal muscle injury

    Atorvastatin: mechanism of action from target occupancy to isoprenoids, transport, muscle and metabolism (2026-09-22) · lines 133–142

    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

    ## slco1b1-variant-and-statin-myopathy A genome-wide association study found a single strong association of statin myopathy with the rs4363657 variant within SLCO1B1, which encodes the hepatic uptake transporter OATP1B1. Model/species: 85 subjects with definite or incipient myopathy and 90 controls, replicated in a separate trial Tissue/system: Hepatic statin uptake and skeletal muscle injury Exposure: Simvastatin 80 mg daily, replication at simvastatin 40 mg daily Route: Oral Duration: Trial duration, not stated here Limits: The statin was simvastatin, not atorvastatin, and the association is with a noncoding variant rather than a demonstrated change in transporter function in these subjects. Primary reference: SLCO1B1 variants and statin-induced myopathy--a genomewide study. (2008). https://pubmed.ncbi.nlm.nih.gov/18650507/ DOI: 10.1056/NEJMoa0801936 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