Impact of Exercise and Aging on Mitochondrial Homeostasis in Skeletal Muscle: Roles of ROS and Epigenetics
Aging causes degenerative changes such as epigenetic changes and mitochondrial dysfunction in skeletal muscle. Exercise can upregulate muscle mitochondrial homeostasis and enhance antioxidant capacity and represents an effective treatment to prevent muscle aging. Epigenetic changes such as DNA methy...
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MDPI AG
2022-06-01
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author | Jialin Li Zhe Wang Can Li Yu Song Yan Wang Hai Bo Yong Zhang |
author_facet | Jialin Li Zhe Wang Can Li Yu Song Yan Wang Hai Bo Yong Zhang |
author_sort | Jialin Li |
collection | DOAJ |
description | Aging causes degenerative changes such as epigenetic changes and mitochondrial dysfunction in skeletal muscle. Exercise can upregulate muscle mitochondrial homeostasis and enhance antioxidant capacity and represents an effective treatment to prevent muscle aging. Epigenetic changes such as DNA methylation, histone posttranslational modifications, and microRNA expression are involved in the regulation of exercise-induced adaptive changes in muscle mitochondria. Reactive oxygen species (ROS) play an important role in signaling molecules in exercise-induced muscle mitochondrial health benefits, and strong evidence emphasizes that exercise-induced ROS can regulate gene expression via epigenetic mechanisms. The majority of mitochondrial proteins are imported into mitochondria from the cytosol, so mitochondrial homeostasis is regulated by nuclear epigenetic mechanisms. Exercise can reverse aging-induced changes in myokine expression by modulating epigenetic mechanisms. In this review, we provide an overview of the role of exercise-generated ROS in the regulation of mitochondrial homeostasis mediated by epigenetic mechanisms. In addition, the potential epigenetic mechanisms involved in exercise-induced myokine expression are reviewed. |
first_indexed | 2024-03-09T22:02:09Z |
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institution | Directory Open Access Journal |
issn | 2073-4409 |
language | English |
last_indexed | 2024-03-09T22:02:09Z |
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spelling | doaj.art-ff3047052c66435a879b60d8fb66c43b2023-11-23T19:49:16ZengMDPI AGCells2073-44092022-06-011113208610.3390/cells11132086Impact of Exercise and Aging on Mitochondrial Homeostasis in Skeletal Muscle: Roles of ROS and EpigeneticsJialin Li0Zhe Wang1Can Li2Yu Song3Yan Wang4Hai Bo5Yong Zhang6Tianjin Key Laboratory of Exercise Physiology and Sports Medicine, Institute of Exercise and Health, Tianjin University of Sport, Tianjin 301617, ChinaTianjin Key Laboratory of Exercise Physiology and Sports Medicine, Institute of Exercise and Health, Tianjin University of Sport, Tianjin 301617, ChinaTianjin Key Laboratory of Exercise Physiology and Sports Medicine, Institute of Exercise and Health, Tianjin University of Sport, Tianjin 301617, ChinaTianjin Key Laboratory of Exercise Physiology and Sports Medicine, Institute of Exercise and Health, Tianjin University of Sport, Tianjin 301617, ChinaTianjin Key Laboratory of Exercise Physiology and Sports Medicine, Institute of Exercise and Health, Tianjin University of Sport, Tianjin 301617, ChinaTianjin Key Laboratory of Exercise Physiology and Sports Medicine, Institute of Exercise and Health, Tianjin University of Sport, Tianjin 301617, ChinaTianjin Key Laboratory of Exercise Physiology and Sports Medicine, Institute of Exercise and Health, Tianjin University of Sport, Tianjin 301617, ChinaAging causes degenerative changes such as epigenetic changes and mitochondrial dysfunction in skeletal muscle. Exercise can upregulate muscle mitochondrial homeostasis and enhance antioxidant capacity and represents an effective treatment to prevent muscle aging. Epigenetic changes such as DNA methylation, histone posttranslational modifications, and microRNA expression are involved in the regulation of exercise-induced adaptive changes in muscle mitochondria. Reactive oxygen species (ROS) play an important role in signaling molecules in exercise-induced muscle mitochondrial health benefits, and strong evidence emphasizes that exercise-induced ROS can regulate gene expression via epigenetic mechanisms. The majority of mitochondrial proteins are imported into mitochondria from the cytosol, so mitochondrial homeostasis is regulated by nuclear epigenetic mechanisms. Exercise can reverse aging-induced changes in myokine expression by modulating epigenetic mechanisms. In this review, we provide an overview of the role of exercise-generated ROS in the regulation of mitochondrial homeostasis mediated by epigenetic mechanisms. In addition, the potential epigenetic mechanisms involved in exercise-induced myokine expression are reviewed.https://www.mdpi.com/2073-4409/11/13/2086agingexerciseROSmitochondrialepigeneticsskeletal muscle |
spellingShingle | Jialin Li Zhe Wang Can Li Yu Song Yan Wang Hai Bo Yong Zhang Impact of Exercise and Aging on Mitochondrial Homeostasis in Skeletal Muscle: Roles of ROS and Epigenetics Cells aging exercise ROS mitochondrial epigenetics skeletal muscle |
title | Impact of Exercise and Aging on Mitochondrial Homeostasis in Skeletal Muscle: Roles of ROS and Epigenetics |
title_full | Impact of Exercise and Aging on Mitochondrial Homeostasis in Skeletal Muscle: Roles of ROS and Epigenetics |
title_fullStr | Impact of Exercise and Aging on Mitochondrial Homeostasis in Skeletal Muscle: Roles of ROS and Epigenetics |
title_full_unstemmed | Impact of Exercise and Aging on Mitochondrial Homeostasis in Skeletal Muscle: Roles of ROS and Epigenetics |
title_short | Impact of Exercise and Aging on Mitochondrial Homeostasis in Skeletal Muscle: Roles of ROS and Epigenetics |
title_sort | impact of exercise and aging on mitochondrial homeostasis in skeletal muscle roles of ros and epigenetics |
topic | aging exercise ROS mitochondrial epigenetics skeletal muscle |
url | https://www.mdpi.com/2073-4409/11/13/2086 |
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