Component
ACSL4
Independent entity for contextual scientific-audit claims; no universal nutritional effect implied.
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.
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
ACSL4 activates arachidonic acid to arachidonoyl-CoA upstream of phospholipid incorporation.
Experimental context and source evidence
- cell_type
- Experimental cell models
- experimental_model
- Cell genetic perturbation, mouse lung epithelial Lpcat3 knockdown, redox lipidomics
- limitations
- Not proof of ACSL4 dependence in every ferroptosis model.
- organism
- Mus musculus
Selenium: literature corrections and mechanism additions · lines 1215–1225
Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Cell genetic perturbation, mouse lung epithelial Lpcat3 knockdown, redox lipidomics · secondary_verified · secondary_verified
## acsl4-activation ACSL4 prepares the fatty acid for membrane incorporation. ACSL4 activates arachidonic acid to arachidonoyl-CoA upstream of phospholipid incorporation. Organism: Mus musculus Cell type: Experimental cell models Experimental model: Cell genetic perturbation, mouse lung epithelial Lpcat3 knockdown, redox lipidomics Limitations: Not proof of ACSL4 dependence in every ferroptosis model. Primary reference: [Oxidized arachidonic and adrenic PEs navigate cells to ferroptosis](https://pubmed.ncbi.nlm.nih.gov/27842066/)
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.