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. 2022 Jan 18;9:774957. doi: 10.3389/fcell.2021.774957

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Copyright © 2022 Ge, Zhang, Mu, Zheng, Tan, Huang, Xu, Zou, Zhu, Feng and Aa.

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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Regulatory networks and signaling pathways associated with ferroptosis. Ferroptosis is primarily activated by iron-dependent lipid peroxidation and redox perturbation, which mainly occurs through two major pathways, the extrinsic or transporter-dependent pathway, and the intrinsic or enzyme-regulated pathway. (A) The cyst(e)ine/GSH/GPX4 antioxidative axis. (B) The mevalonate pathway (IPP/FSP1/CoQ10 system). (C) NRF2-regulated ARE defence. (D) The glutaminolysis pathway. (E) The lipid peroxidation process; (F) The absorption, export, storage and utilization of iron. (G) The autophagy cascade. (H) The EMT-related pathway. Processes favoring or counteracting ferroptotic cell death are labeled with red and green arrows, respectively (Cys₂, cystine; Cys, cysteine; Glu, glutamate; Gly, glycine Gln, glutamine; BCNU, 1,3-bis-(2-chloroethyl)-1-nitrosourea; CoQ10H2, ubiquinol; HMG-CoA, 3-hydroxy-3-methyl glutaryl coenzyme A; GSR, glutathione-disulfide reductase; BHA, butylated hydroxyanisole; BHT, butylated hydroxytoluene).