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. 2020 May 21;11:2549. doi: 10.1038/s41467-020-16312-7

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© The Author(s) 2020

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. 10 — In this model, PGAM5 regulates senescence through several mechanisms. First, PGAM5 is required for regulating mitochondrial dynamics. PGAM5 deletion leads to elevation of Drp1 phosphorylation at Ser-637, which tip the balance of mitochondrial dynamics toward hyperfusion and less mitochondrial turnover. As result, this results in elevated ATP and ROS production, activation of AMPK–mTOR pathway, and accelerated senescence. Second, PGAM5 deletion promotes the IRF/IFN-β pathway, which could also contribute to cell senescence. PGAM5 deletion leads to resistance to oxidative stress, possibly through mitochondrial hyperfusion and/or upregulation of anti-oxidative genes. This resistance is lost in aging possibly due to the accelerated senescence caused by PGAM5 deletion. Our model highlights a critical role for PGAM5 in regulating mitochondrial dynamics, senescence and age-related oxidative response.