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. 2023 Aug 23;55(8):1632–1643. doi: 10.1038/s12276-023-01069-y

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© The Author(s) 2023

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. 4 — Ferroptosis is primarily driven by iron-dependent lipid peroxidation. Iron bound to transferrin is transported into cells by TFRC1. NCOA4-mediated ferritinophagy increases the free iron pool. Ferroptosis is inhibited by GSH, the synthesis of which involves the uptake of cystine via the cystine-glutamate antiporter (system X_c^-). Using GSH as a cofactor, GPX4 reduces phospholipid hydroperoxides to their corresponding alcohols. The FSP1-CoQ10 system inhibits ferroptosis.