Forkhead Box O Signaling Pathway in Skeletal Muscle Atrophy

被引:67
作者
Chen, Kun [1 ]
Gao, Peng [1 ]
Li, Zongchao [1 ]
Dai, Aonan [1 ]
Yang, Ming [1 ]
Chen, Siyu [2 ,3 ]
Su, Jingyue [2 ,3 ]
Deng, Zhenhan [2 ,3 ]
Li, Liangjun [1 ]
机构
[1] Univ South China, Affiliated Changsha Cent Hosp, Hengyang Med Sch, Dept Orthopaed, Changsha, Hunan, Peoples R China
[2] Shenzhen Univ, Shenzhen Peoples Hosp 2, Affiliated Hosp 1, Dept Sports Med, Shenzhen, Guangdong, Peoples R China
[3] Guangxi Univ Chinese Med, Sch Med, Nanning, Peoples R China
关键词
FOXO TRANSCRIPTION FACTORS; UBIQUITIN LIGASES; PROTEIN-DEGRADATION; THERAPEUTIC TARGETS; NUCLEAR EXCLUSION; GENE-EXPRESSION; VITAMIN-D; AUTOPHAGY; AXIS; AKT;
D O I
10.1016/j.ajpath.2022.09.003
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Skeletal muscle atrophy is the consequence of protein degradation exceeding protein synthesis because of disease, aging, and physical inactivity. Patients with skeletal muscle atrophy have decreased muscle mass and fiber cross-sectional area, and experience reduced survival quality and motor function. The forkhead box O (FOXO) signaling pathway plays an important role in the pathogenesis of skeletal muscle atrophy by regulating E3 ubiquitin ligases and some autophagy factors. However, the mechanism of FOXO signaling pathway leading to skeletal muscle atrophy is still unclear. The development of treatment strategies for skeletal muscle atrophy has been a thorny clinical problem. FOXO-targeted therapy to treat skeletal muscle atrophy is a promising approach, and an increasing number of relevant studies have been reported. This article reviews the mechanism and therapeutic targets of the FOXO signaling pathway mediating skeletal muscle atrophy, and provides ideas for the clinical treatment of this condition.
引用
收藏
页码:1648 / 1657
页数:10
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