Ferroptosis is an iron- and ROS-dependent form of regulated cell death (RCD). Ferroptosis is distinct from other forms of RCD at morphological, biochemical, and genetic levels. It is characterized morphologically by the presence of smaller than normal mitochondria with condensed mitochondrial membrane densities, reduction or vanishing of mitochondria crista, and outer mitochondrial membrane rupture. It can be induced by experimental compounds (e.g., erastin, Ras-selective lethal small molecule, and buthionine sulfoximine) or clinical drugs (e.g., sulfasalazine, sorafenib, and artesunate) in cancer cells and certain normal cells. Several molecules (e.g., VDAC2/3, glutathione peroxidase (GPX4), heat shock protein beta-1 (HSPB1), nuclear factor E2-related factor 2 (NRF2), NADPH oxidase (NOX), p53, and SLC7A11) regulate ferroptosis by directly or indirectly targeting iron metabolism and lipid peroxidation. Misregulated ferroptosis has been implicated in multiple physiological and pathological processes such as cancer cell death, tissue injury, and T-cell immunity.


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