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. 2022 Jul 22;10:947357. doi: 10.3389/fcell.2022.947357

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Copyright © 2022 Yapryntseva, Maximchik, Zhivotovsky and Gogvadze.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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(A) Sirtuin 3 and apoptosis. Sirt3 suppresses excessive production of ROS, which can stimulate OMM permeabilization through oxidation of thiols in ANT or Bax. In addition, Sirt3 deacetylates CypD, preventing pore opening, and modulates OMM permeabilization mediated by Bcl-2 family proteins, although the mechanisms of these processes are still poorly understood. Red arrows denote pro-apoptotic effects and green arrows denote anti-apoptotic effects. (B) Sirtuin 3 and necroptosis. Sirt3 inhibits mitochondrial ROS production and prevents MPT pore opening which can be involved in necroptosis. Sirt3 also deacetylates p53 which promotes necroptosis in mitochondria-independent way. LncRNAs—long non-coding RNAs. Red arrows denote pro-necroptotic effects and green arrows denote anti-necroptotic effects. (C) Sirtuin 3 and autophagy. Sirt3 promotes autophagy via AMPK and FOXO1 activation. It also stimulates expression of autophagy-related genes via FOXO3a deacetylation. Sirt3 can inhibit autophagy via suppression of ROS-dependent AMPK-pathway stimulation and via acetyl-CoA pools maintaining. Green arrows denote pro-autophagic effects and red arrows denote anti-autophagic effects. (D) Sirtuin 3 and mitophagy. Sirt3 stimulates PINK1/Parkin-dependent as well as receptor-mediated mitophagy. Sirt3 also promotes mitochondrial fission which is a prerequisite of mitophagy. Green arrows denote pro-mitophagic effects.