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. 2024 Mar 5;20(6):1213–1246. doi: 10.1080/15548627.2024.2319901

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© 2024 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 5. — Mitophagy in ferroptosis. Mitophagy is a selective process that involves the autophagic clearance of damaged or dysfunctional mitochondria. The PINK1-PRKN pathway is a well-studied regulatory pathway for mitophagy. In this pathway, PINK1 recruits PRKN, which facilitates the degradation of mitochondria through mitophagy receptors such as FUNDC1. Mitochondrial fission induced by DNM1L/Drp1 can promote mitophagy-dependent ferroptosis. Additionally, the mitochondrial protein FTMT inhibits ROS production and ferroptosis.