Ferroptosis

Ferroptosis

Ferroptosis is regarded as a cell death modality of metabolism. The biochemical mechanisms of ferroptosis involve a complex interaction between oxidative stress, lipid metabolism, and iron homeostasis that results in the peroxidation of polyunsaturated fatty acid (PUFA)-containing phospholipids to produce phospholipid peroxide radicals. These lipid peroxide radicals can react with other PUFAs that, in turn, generate additional peroxide radicals, which propagate as a chain-reaction throughout the phospholipid bilayer, leading to cell rupture. Briefly, ferroptosis-prone PUFAs contain bis-allylic hydrogen atoms that are liable to removal from the PUFA scaffold, exposing carbon moieties that can react with ferric iron or oxygen radicals either directly, or subsequent to attachment of molecular oxygen, form lipid (hydro)peroxides. The oxidation of PUFAs in the cell membrane can be initiated by reactive oxygen species (ROS) such as hydroxyl radicals, which can be generated by labile iron in the Fenton reaction. Hence, iron levels are strictly regulated by a variety of storage, transport and export proteins, including ferritin, transferrin, hepcidin, ferroportin and transferrin receptor 1 (TFR1) to avoid excess iron-derived ROS generation. Yet, the peroxidation of PUFAs is unavoidable, and this would result in ferroptosis if not continually interdicted by cellular defences. Thus, ferroptosis is distinct from other cell death modalities, where the initiation of cell death is an active event (e.g., apoptosis); ferroptosis, rather, usually is initiated by the withdrawal of cellular antioxidant defences.

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