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Cells can die in several programmed ways. Beyond the classic apoptosis, ferroptosis kills through iron-driven fat oxidation, and drug-resistant, mesenchymal cancer cells turn out to be unusually prone to it.
Ferroptosis is iron-dependent lipid peroxidation restrained by GPX4 (using glutathione from the cystine transporter SLC7A11/xCT) and by FSP1. Therapy-persistent, mesenchymal, and dedifferentiated cancer cells depend on GPX4; radiation and some immunotherapies act partly via ferroptosis. Necroptosis (RIPK3/MLKL) and pyroptosis (gasdermins) are inflammatory death modes that can be immunogenic. No ferroptosis inducer is approved; GPX4 inhibitors lack drug-like properties, so xCT inhibition, cyst(e)inase, and sulfasalazine repurposing are the clinical routes.
Ferroptosis is rust. Iron plus oxygen eats through the cell's membranes unless an antioxidant crew (GPX4) keeps repainting them. Cells that changed shape to dodge chemotherapy have thinner paint.
One pathway page on OnCo cites this paper by its DOI; this record gives the citation a page of its own so a reader can follow it without leaving OnCo. Read the abstract above alongside the citing page listed under Related; the record was created automatically from the Europe PMC entry and its figures have not been checked by hand.
One pathway page on OnCo cites this paper by its DOI; this record gives the citation a page of its own so a reader can follow it without leaving OnCo. Read the abstract above alongside the citing page listed under Related; the record was created automatically from the Europe PMC entry and its figures have not been checked by hand.
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