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. 2021 Aug 13;9:699304. doi: 10.3389/fcell.2021.699304

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Copyright © 2021 Wang, Wang, Li, Qin and Wang.

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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Lipid peroxidation in ferroptosis. The increased absorption of cysteine in tumor cells is utilized to build up the cysteine–glutathione (GSH)–GPX4 axis, which plays a crucial role in detoxifying cellular oxidants and evading ferroptosis. Acyl-CoA synthetase long-chain family member 4 (ACSL4) associates with lysophosphatidylcholine acyltransferase 3 (LPCTA3) to incorporate polyunsaturated fatty acids (PUFAs) into PL-PUFA (PE), which shows higher susceptibility to peroxidation and ferroptosis. The catalytic iron inside cells appears to be the source of Fenton chemistry, which creates hydroxyl and peroxyl radicals capturing hydrogen atoms from PUFAs and triggering peroxidation of PL-PUFA. FSP1, a novel finding of ferroptosis suppressor, protects cells against ferroptosis by catalyzing the regeneration of CoQ10 using NAD(P)H. FIN56 induces ferroptosis by promoting the GPX4 degradation and lowering the CoQ10 amount.