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. 2022 Sep 20;8:394. doi: 10.1038/s41420-022-01183-2

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — Ferroptosis is caused by excessive accumulation of lipid peroxide, ROS production and abnormal iron metabolism. Excessive Fe²⁺ accumulation will cause ROS production and lipid peroxidation. System Xc⁻ can control the transport of cystine to cells and affect GPX4 activity. GPX4 is a key molecule for endogenous inhibition of lipid peroxidation. The arrows indicate promotion, and the blunt-ended lines indicate inhibition. STEAP3 six-transmembrane epithelial antigen of prostate 3, DMT1 divalent metal transporter 1, TfR1 transferrin receptor 1, GSSG glutathione disulfide, ROS reactive oxygen species, LOOH lipid peroxides.