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. 2017 Mar 30;8(3):e2716. doi: 10.1038/cddis.2017.133

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Copyright © 2017 The Author(s)

Cell Death and Disease is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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Proposed mechanistic model and experimental evidence. Treatment with BAY inhibits mitochondrial CI. This induces a (local) increase in reactive oxygen species (ROS) levels (‘triggering ROS'), which stimulates mPTP opening and autophagosome formation. Simultaneously, CI inhibition induces depolarization of the mitochondrial membrane potential (Δψ) leading to mitophagy induction. The latter increases ROS levels (‘killing ROS') leading to parallel stimulation of necrosome formation (RIPK1/MLKL), lipid peroxidation and GSH depletion. Increased necrosome formation further stimulates ROS levels and leads to induction of necroptosis, whereas lipid peroxidation and GSH depletion stimulate ferroptosis. Experimental evidence presented in this study are marked in red (inhibitory effect) and green (stimulatory effect)