Mitochondrial dysfunction: roles in skeletal muscle atrophy

被引:121
作者
Chen, Xin [1 ]
Ji, Yanan [1 ]
Liu, Ruiqi [2 ]
Zhu, Xucheng [2 ]
Wang, Kexin [1 ]
Yang, Xiaoming [1 ]
Liu, Boya [1 ]
Gao, Zihui [1 ]
Huang, Yan [2 ]
Shen, Yuntian [1 ]
Liu, Hua [3 ]
Sun, Hualin [1 ]
机构
[1] Nantong Univ, Affiliated Hosp, Coinnovat Ctr Neuroregenerat,NIMPA Key Lab Res & E, Dept Neurol,Jiangsu & Minist Educ,Key Lab Neuroreg, Nantong 226001, Jiangsu, Peoples R China
[2] Nantong Univ, Med Coll, Dept Clin Med, Nantong 226001, Jiangsu, Peoples R China
[3] Haian Hosp Tradit Chinese Med, Dept Orthoped, 55 Ninghai Middle Rd, Nantong 226600, Jiangsu, Peoples R China
基金
中国国家自然科学基金;
关键词
Mitochondrial dysfunction; Muscle atrophy; Therapy; Antioxidants; UBIQUITIN-PROTEASOME SYSTEM; OXIDATIVE STRESS; PROTEIN-DEGRADATION; AEROBIC EXERCISE; RESISTANCE EXERCISE; SIGNALING PATHWAY; REDOX REGULATION; AUTOPHAGY; SARCOPENIA; DENERVATION;
D O I
10.1186/s12967-023-04369-z
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Mitochondria play important roles in maintaining cellular homeostasis and skeletal muscle health, and damage to mitochondria can lead to a series of pathophysiological changes. Mitochondrial dysfunction can lead to skeletal muscle atrophy, and its molecular mechanism leading to skeletal muscle atrophy is complex. Understanding the pathogenesis of mitochondrial dysfunction is useful for the prevention and treatment of skeletal muscle atrophy, and finding drugs and methods to target and modulate mitochondrial function are urgent tasks in the prevention and treatment of skeletal muscle atrophy. In this review, we first discussed the roles of normal mitochondria in skeletal muscle. Importantly, we described the effect of mitochondrial dysfunction on skeletal muscle atrophy and the molecular mechanisms involved. Furthermore, the regulatory roles of different signaling pathways (AMPK-SIRT1-PGC-1 & alpha;, IGF-1-PI3K-Akt-mTOR, FoxOs, JAK-STAT3, TGF-& beta;-Smad2/3 and NF-& kappa;B pathways, etc.) and the roles of mitochondrial factors were investigated in mitochondrial dysfunction. Next, we analyzed the manifestations of mitochondrial dysfunction in muscle atrophy caused by different diseases. Finally, we summarized the preventive and therapeutic effects of targeted regulation of mitochondrial function on skeletal muscle atrophy, including drug therapy, exercise and diet, gene therapy, stem cell therapy and physical therapy. This review is of great significance for the holistic understanding of the important role of mitochondria in skeletal muscle, which is helpful for researchers to further understanding the molecular regulatory mechanism of skeletal muscle atrophy, and has an important inspiring role for the development of therapeutic strategies for muscle atrophy targeting mitochondria in the future.
引用
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页数:24
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