Component
Endothelial cell death
Loss of endothelial viability; tissue and causative manipulation are specified per record.
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 acts on it
Six weeks of vitamin E-depleted diet before inducible endothelial Gpx4 deletion led to endothelial detachment and cell death in multiple mouse organs, accompanied by thrombosis and approximately 80% knockout mortality.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- cross_nutrient
- true
- evidence_location
- Primary abstract
- experimental_model
- Combined dietary depletion and 4-hydroxytamoxifen-induced deletion
- exposure
- Six-week vitamin E depletion preceding Gpx4 deletion.
- limitations
- Primary abstract only; vascular and survival endpoints in one mouse deletion model, not general human deficiency or dosing evidence.
- nutrient_topic
- Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
- organism
- Mus musculus
- plain_language
- Removing dietary vitamin E exposed severe vascular injury in mice whose endothelial GPX4 was then deleted.
- primary_references
- [ver-wortmann2013] Combined deficiency in glutathione peroxidase 4 and vitamin E causes multiorgan thrombus formation and early death in mice. (2013). https://pubmed.ncbi.nlm.nih.gov/23770613/ DOI: 10.1161/circresaha.113.279984
- tissue_or_cell_type
- Multiorgan vascular endothelium
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 648–660
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Combined dietary depletion and 4-hydroxytamoxifen-induced deletion · source_derived_draft · unverified_draft
### ver-endo-combined-e-gpx4-loss Six weeks of vitamin E-depleted diet before inducible endothelial Gpx4 deletion led to endothelial detachment and cell death in multiple mouse organs, accompanied by thrombosis and approximately 80% knockout mortality. Condition category: nutrient_deficiency nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing dietary vitamin E exposed severe vascular injury in mice whose endothelial GPX4 was then deleted. organism: Mus musculus tissue_or_cell_type: Multiorgan vascular endothelium experimental_model: Combined dietary depletion and 4-hydroxytamoxifen-induced deletion limitations: Primary abstract only; vascular and survival endpoints in one mouse deletion model, not general human deficiency or dosing evidence. exposure: Six-week vitamin E depletion preceding Gpx4 deletion. cross_nutrient: true evidence_location: Primary abstract [ver-wortmann2013] Combined deficiency in glutathione peroxidase 4 and vitamin E causes multiorgan thrombus formation and early death in mice. (2013). https://pubmed.ncbi.nlm.nih.gov/23770613/ DOI: 10.1161/circresaha.113.279984
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.