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. 2023 Sep 28;20(3):469–488. doi: 10.1080/15548627.2023.2259732

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© 2023 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License (http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way. The terms on which this article has been published allow the posting of the Accepted Manuscript in a repository by the author(s) or with their consent.

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Figure 3. — Lipid mechanism in ferroptosis. Ferroptosis is regulated by antioxidant enzymes, including GPX4 and AIFM2, which play a role in reducing ubiquinone (coenzyme Q10) and inhibiting ferroptosis. Among lipids, polyunsaturated fatty acids (PUFAs) are highly susceptible to peroxidation during ferroptosis. Long-chain saturated fatty acids (SFAs), such as palmitic acid (PA, C16:0) and stearic acid (SA, C18:0), as well as their downstream fatty alcohols (1-hexadecanol and 1-octadecanol), sensitize RSL3-induced ferroptosis. Conversely, exogenous monounsaturated fatty acids (MUFAs), including oleic acid (OA, C18:1) and palmitoleic acid (POA, C16:1), suppress ferroptosis. The regulation of key lipid metabolic enzymes involved in lipid synthesis, degradation, storage, transformation, and utilization is crucial in the context of ferroptosis. AA: arachidonic acid, AdA: adrenic acid, DHA: docosahexaenoic acid, DPA: docosapolyenoic acid, 1-HE: 1-hexadecanol, 1-OE: 1-octadecanol, eLPE/LPC: ether lysophosphatidylethanolamine/lysophosphocholine, ePe/epc: ether phosphatidylethanolamine/phosphocholine.