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. 2021 Mar 25;9:646890. doi: 10.3389/fcell.2021.646890

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Copyright © 2021 Chen, Kang and Tang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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The mechanism of lipid peroxidation in ferroptosis. Excessive lipid peroxidation plays an important role in promoting ferroptosis by producing toxic PLOOH. At least three pathways mediated by POR/CYB5R1, NOX, and ALOX contribute to PLOOH production. In contrast, activation of the SLC7A11-GSH-GPX4, AIFM2-CoQ10, GCH1-BH4 axis limits lipid peroxidation during ferroptosis. In addition, PLOOH-mediated membrane damage can be repaired by the ESCRT-III membrane scission complex. ACSL4, acyl-CoA synthetase long-chain family member 4; AIFM2/FSP1, apoptosis inducing factor mitochondria associated 2; BH4, tetrahydrobiopterin; CoQ10, coenzyme Q10; CYB5R1, cytochrome B5 reductase 1; ESCRT-III, endosomal sorting complex required for transport-III; GCH1, GTP cyclohydrolase 1; GPX4, glutathione peroxidase 4; GSH, glutathione; H₂O₂, hydrogen peroxide; PLOOH, phospholipid hydroperoxide; POR, cytochrome P450 oxidoreductase; PUFA, polyunsaturated fatty acids; LPCAT3, lysophosphatidylcholine acyltransferase 3; ALOX, lipoxygenase; NOX, NADPH oxidases; PUFA-PL, polyunsaturated phospholipids; SLC7A11, solute carrier family 7 member 11.