期刊
CELLS
卷 11, 期 13, 页码 -出版社
MDPI
DOI: 10.3390/cells11132086
关键词
aging; exercise; ROS; mitochondrial; epigenetics; skeletal muscle
类别
资金
- National Natural Science Foundation of China [31771320, 32071177, 31571224]
- Tianjin Scientific Research Foundation [19JCYBJC25000]
- Tianjin Research Innovation Project for Postgraduate Students [2021YJSB375]
- Scientific Research Project of Tianjin Municipal Education Commission [2021KJ002]
Exercise can prevent muscle aging by regulating mitochondrial homeostasis and antioxidant capacity. Epigenetic changes and mitochondrial dysfunction are the main causes of muscle aging, and exercise can reverse these changes by modulating epigenetic mechanisms.
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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据