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. 2023 Aug 14;14(8):519. doi: 10.1038/s41419-023-06045-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. 3 — AMPK is the energy sensor, cancer cells with high basal AMPK activation are resistant to ferroptosis and AMPK inactivation sensitizes these cells to ferroptosis. Mechanistically, AMPK regulates ferroptosis through acetyl-CoA carboxylase (ACC) and polyunsaturated fatty acid (PUFA) biosynthesis. TCA metabolites such as α-KG and its downstream products succinic acid and fumaric acid could all enhance the ferroptosis induced by cysteine depletion.