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. 2021 Sep 27;11:19116. doi: 10.1038/s41598-021-98771-6

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© The Author(s) 2021

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Proposed pathway of TMZ effects on HFD-induced muscle dysfunction. Mitochondrial quality control (MQC) including mitochondrial biogenesis, dynamics, and autophagy cooperate to ensure mitochondrial homeostasis. Mitochondrial dysfunction arising from impaired mitochondrial quality control is critically involved in the pathogenesis of muscle atrophy. During high-fat diet (HFD)-induced obesity, adversely alteration in atrophic factors (i.e. Atrogin-1/MAFbx and MuRF1) and MQC were observed. However, our data shows exercise training or TMZ treatment enhances MQC and suppresses atrophic factors to alleviate HFD-induced muscle dysfunction. Thus, we conclude that TMZ might be a potential therapy in the treatment of muscle atrophy in addition to exercise against HFD-induced muscle dysfunction.