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. 2021 Jul 22;8:710963. doi: 10.3389/fcvm.2021.710963

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Copyright © 2021 Hu, Chen, Jing, Zhai and Shen.

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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Schematic description of the mechanisms of ferroptosis. Ferroptosis is a type of regulated cell death characterized by iron overload and lipid peroxidation. Fe³⁺ is transferred into the cell by TfR1, then converted to Fe²⁺ in the endosome, and released from the endosome by divalent metal transporter 1 (DMT1). Fenton reaction promotes lipid peroxidation by activating lipoxygenases (LOXs). Cystine is uptaken by system xc⁻ for the synthesis of GSH, which further enhances the anti-lipid peroxidation activity of GPX4. In addition, FSP1-CoQ10 and GCH1-BH4/BH2 are two parallel GPX4-independent pathways in the suppression of ferroptosis. TfR1, transferrin receptor 1; STEAP3, STEAP family member 3; Hmox1, heme oxygenase-1; BSO, buthionine sulfoximine; PUFA, polyunsaturated fatty acid; CoA, coenzyme A; PL, lysophosphatide; ACSL4, acyl-CoA synthetase long-chain family member 4; LPCAT3, lysophosphatidylcholine acyltransferase 3; LOOH, polyunsaturated fatty acid hydroperoxides; GSH, glutathione; SLC7A11, solute carrier family 7 member 11; SLC3A2, solute carrier family 3 member 2; FSP1, ferroptosis suppressor protein1; ESCRT-III, endosomal sorting complex required for transport-III; GCH-1, guanosine triphosphate cyclohydrolase 1; BH4/BH2, tetrahydrobiopterin/dihydrobiopterin.