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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. 5 — This figure illustrates the crucial processes of mitoptosis and mitophagy that maintain mitochondrial quality and prevent cell pathology. A Mitoptosis is characterized by several events, including mitochondrial fission, the clustering of spherical mitochondria in the perinuclear area, enwrapping of these clusters by a membrane to form a “mitoptotic body,” decomposition of mitochondria into small vesicles, protrusion of the body from the cell, and disruption of the boundary membrane. This process is driven by mitochondrial dysfunction and reactive oxygen species (ROS) production. B Mitophagy is a selective autophagic mechanism for the degradation of damaged or unnecessary mitochondria. This procedure requires activation of general autophagy and priming of injured mitochondria via the Pink1/Parkin signaling pathway. Autophagosomes engulf targeted mitochondria, which are then digested and degraded in lysosomes.