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. 2023 Aug 23;55(8):1573–1594. doi: 10.1038/s12276-023-01078-x

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© The Author(s) 2023, corrected publication 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. 14 — This figure illustrates the key features of oxeiptosis. Oxeiptosis is activated in response to oxidative stress induced by ROS or ROS-generating agents, such as viral pathogens. The KEAP1/PGAM5/AIFM1 signaling pathway plays a central role in oxeiptosis, in which AIFM1 is dephosphorylated under oxidative stress conditions via the regulatory action of PGAM5. Dephosphorylated AIFM1 is translocated from mitochondria to the nucleus, leading to chromatin condensation and DNA fragmentation, ultimately resulting in cell death.