Component
Rat glutathione peroxidase 4 / Gpx4
Context-specific entity; species, compartment and exposure are stated on each claim.
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 acts on it
Fisetin restored GPX4 protein and glutathione while reducing lipid-oxidation markers in doxorubicin-exposed rat hearts and H9c2 cells.
Experimental context and source evidence
- evidence_access
- Primary full text
- experimental_model
- Rat model; H9c2 assays used 40 micromolar fisetin with 1 micromolar doxorubicin for 24 hours.
- limitations
- Does not establish selenium replacement or preservation of anticancer efficacy.
- nutrient_topic
- Fisetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Fisetin
- plain_language
- A selenium-containing defense pathway accompanied protection.
- primary_references
- Fisetin Attenuates Doxorubicin-Induced Cardiomyopathy In Vivo and In Vitro by Inhibiting Ferroptosis Through SIRT1/Nrf2 Signaling Pathway Activation. · 2021 · https://pubmed.ncbi.nlm.nih.gov/35273493/ · DOI 10.3389/fphar.2021.808480
Fisetin: metabolism, cell-state responses and cross-nutrient mechanisms (2026-09-19) · lines 416–422
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat model; H9c2 assays used 40 micromolar fisetin with 1 micromolar doxorubicin for 24 hours. · source_derived_draft · unverified_draft
## fisetin-cardiac-gpx4 A selenium-containing defense pathway accompanied protection. Fisetin restored GPX4 protein and glutathione while reducing lipid-oxidation markers in doxorubicin-exposed rat hearts and H9c2 cells. Model: Rat model; H9c2 assays used 40 micromolar fisetin with 1 micromolar doxorubicin for 24 hours. Limitations: Does not establish selenium replacement or preservation of anticancer efficacy. Evidence access: Primary full text Fisetin Attenuates Doxorubicin-Induced Cardiomyopathy In Vivo and In Vitro by Inhibiting Ferroptosis Through SIRT1/Nrf2 Signaling Pathway Activation. · 2021 · https://pubmed.ncbi.nlm.nih.gov/35273493/ · DOI 10.3389/fphar.2021.808480
Complete structured claim and evidence
Where it participates (unsigned role)
SIRT1 inhibition attenuated fisetin protection in doxorubicin-exposed H9c2 cells and reduced the associated GSH/GPX4 response.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Rat cardiac-cell pharmacological inhibition.
- limitations
- Not proof that niacin or NAD supplements enhance fisetin.
- nutrient_topic
- Fisetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Fisetin
- plain_language
- An intact regulatory pathway was required for the full response.
- primary_references
- Fisetin Attenuates Doxorubicin-Induced Cardiomyopathy In Vivo and In Vitro by Inhibiting Ferroptosis Through SIRT1/Nrf2 Signaling Pathway Activation. · 2021 · https://pubmed.ncbi.nlm.nih.gov/35273493/ · DOI 10.3389/fphar.2021.808480
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Fisetin: metabolism, cell-state responses and cross-nutrient mechanisms (2026-09-19) · lines 432–438
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat cardiac-cell pharmacological inhibition. · source_derived_draft · unverified_draft
## fisetin-cardiac-sirt1-block An intact regulatory pathway was required for the full response. SIRT1 inhibition attenuated fisetin protection in doxorubicin-exposed H9c2 cells and reduced the associated GSH/GPX4 response. Model: Rat cardiac-cell pharmacological inhibition. Limitations: Not proof that niacin or NAD supplements enhance fisetin. Evidence access: Primary abstract Fisetin Attenuates Doxorubicin-Induced Cardiomyopathy In Vivo and In Vitro by Inhibiting Ferroptosis Through SIRT1/Nrf2 Signaling Pathway Activation. · 2021 · https://pubmed.ncbi.nlm.nih.gov/35273493/ · DOI 10.3389/fphar.2021.808480
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.