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. 2023 Apr 15;9:128. doi: 10.1038/s41420-023-01430-0

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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. 1 — Ferroptosis is mainly caused by iron-related lipid peroxidation, and the absorption, storage, utilization and export of iron in iron metabolism will affect ferroptosis. STAMP2-mediated ferric iron reduction and NCOA4-mediated ferritin autophagy can increase labile iron pools to sensitize cells to ferroptosis via the Fenton response. The classical inhibitory pathway of ferritin metabolism is mainly uptake of Cys by the cystine-glutamate antiporter (system xc⁻), which is used for the synthesis of GSH. GPX4 utilizes GSH as a cofactor to reduce lipid hydroperoxides to lipid alcohols. In addition, the activation of ACSL4, LPLAT5, and LOXs in the lipid metabolism pathway can promote the peroxidation of PUFA and induce ferroptosis. Conversely, the PI3K/AKT/mTOR pathway is able to promote SREBP1/SCD1-mediated MUFA formation and convert MUFAs to their acyl-CoA esters under the action of ACSL3 for incorporation into membrane phospholipids, thereby protecting cancer cells from ferroptosis.