Summary
Ferroptosis is an iron-dependent cell death, which is different from apoptosis, necrosis, autophagy, and other forms of cell death. The process of ferroptotic cell death is defined by the accumulation of lethal lipid species derived from the peroxidation of lipids, which can be prevented by iron chelators (e.g., deferiprone, deferoxamine) and small lipophilic antioxidants (e.g., ferrostatin, liproxstatin). This review summarizes current knowledge about the regulatory mechanism of ferroptosis and its association with several pathways, including iron, lipid, and cysteine metabolism. We have further discussed the contribution of ferroptosis to the pathogenesis of several diseases such as cancer, ischemia/reperfusion, and various neurodegenerative diseases (e.g., Alzheimer's disease and Parkin
Regional applicability
This is a mechanistic cell biology review without geographical specificity or agricultural/food-system components. The findings are relevant to clinical and biomedical research internationally, but have no direct applicability to United Kingdom farming systems, soil health, or food-chain interventions.
Key measures
Ferroptosis mechanisms; iron chelation; lipid peroxidation; antioxidant effects; disease associations (cancer, neurodegeneration, ischaemic injury)
Outcomes reported
The review summarises regulatory mechanisms of ferroptosis and its association with iron, lipid, and cysteine metabolism pathways. It evaluates ferroptosis as a pathogenic contributor to cancer, ischaemia/reperfusion injury, and neurodegenerative diseases, and assesses therapeutic potential of ferroptosis inhibitors.
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