Component
Statin therapy as a drug class
Class-level exposure where a finding was not attributed to one statin.
2 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 it acts on
Statin treatment reduced host protein prenylation including prenylation of Rho GTPases, and reduced respiratory syncytial virus infection in vitro through combined cholesterol and isoprenoid effects.
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
- Live-cell high-content screen in human cell culture
- exposure
- Statins, and separately perillyl alcohol as a geranylgeranyltransferase inhibitor
- limitations
- The screen tested statins as a class without attributing the result to atorvastatin, and respiratory syncytial virus infection itself globally upregulated prenylation, so the baseline was not a resting cell.
- organism
- Live-cell high-content screen in human cell culture
- plain_language
- Statin treatment reduced host protein prenylation including prenylation of Rho GTPases, and reduced respiratory syncytial virus infection in vitro through combined cholesterol and isoprenoid effects.
- primary_references
- Statin-mediated disruption of Rho GTPase prenylation and activity inhibits respiratory syncytial virus infection. (2021). https://pubmed.ncbi.nlm.nih.gov/34716403/ DOI: 10.1038/s42003-021-02754-2
- route
- In vitro
- tissue
- Host protein prenylation and virus production
Atorvastatin: mechanism of action from target occupancy to isoprenoids, transport, muscle and metabolism (2026-09-22) · lines 89–98
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-reduces-rho-gtpase-prenylation Statin treatment reduced host protein prenylation including prenylation of Rho GTPases, and reduced respiratory syncytial virus infection in vitro through combined cholesterol and isoprenoid effects. Model/species: Live-cell high-content screen in human cell culture Tissue/system: Host protein prenylation and virus production Exposure: Statins, and separately perillyl alcohol as a geranylgeranyltransferase inhibitor Route: In vitro Duration: Not stated here Limits: The screen tested statins as a class without attributing the result to atorvastatin, and respiratory syncytial virus infection itself globally upregulated prenylation, so the baseline was not a resting cell. Primary reference: Statin-mediated disruption of Rho GTPase prenylation and activity inhibits respiratory syncytial virus infection. (2021). https://pubmed.ncbi.nlm.nih.gov/34716403/ DOI: 10.1038/s42003-021-02754-2 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
Complete structured claim and evidenceStatin therapy was associated with a 9 percent increased risk of incident diabetes across 13 randomised trials.
Experimental context and source evidence
- duration
- Mean 4 years
- evidence_access
- Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
- experimental_model
- Meta-analysis of 13 statin trials with 91,140 participants, of whom 4,278 developed diabetes
- exposure
- Statin therapy in trials of more than 1,000 patients lasting more than one year
- limitations
- A class-level association across statins and doses, not an atorvastatin-specific or mechanism-specific result, and derived from trials whose primary endpoints were cardiovascular.
- organism
- Meta-analysis of 13 statin trials with 91,140 participants, of whom 4,278 developed diabetes
- plain_language
- Statin therapy was associated with a 9 percent increased risk of incident diabetes across 13 randomised trials.
- primary_references
- Statins and risk of incident diabetes: a collaborative meta-analysis of randomised statin trials. (2010). https://pubmed.ncbi.nlm.nih.gov/20167359/ DOI: 10.1016/S0140-6736(09)61965-6
- route
- Oral
- tissue
- New-onset diabetes mellitus
Atorvastatin: mechanism of action from target occupancy to isoprenoids, transport, muscle and metabolism (2026-09-22) · lines 188–197
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-therapy-and-incident-diabetes Statin therapy was associated with a 9 percent increased risk of incident diabetes across 13 randomised trials. Model/species: Meta-analysis of 13 statin trials with 91,140 participants, of whom 4,278 developed diabetes Tissue/system: New-onset diabetes mellitus Exposure: Statin therapy in trials of more than 1,000 patients lasting more than one year Route: Oral Duration: Mean 4 years Limits: A class-level association across statins and doses, not an atorvastatin-specific or mechanism-specific result, and derived from trials whose primary endpoints were cardiovascular. Primary reference: Statins and risk of incident diabetes: a collaborative meta-analysis of randomised statin trials. (2010). https://pubmed.ncbi.nlm.nih.gov/20167359/ DOI: 10.1016/S0140-6736(09)61965-6 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
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.