Advances in research on cell models for skeletal muscle atrophy

被引:7
|
作者
Li, Liwei [1 ]
Huang, Chunman [1 ]
Pang, Jingqun [1 ]
Huang, Yongbin [1 ]
Chen, Xinxin [2 ]
Chen, Guanghua [3 ]
机构
[1] Guangdong Med Univ, Wenming East Rd 2, Zhanjiang 524000, Guangdong, Peoples R China
[2] Guangdong Med Univ, Affliated Hosp, Inst Hlth Promot & Med Commun Studies, South Renmin Rd 57, Zhanjiang 524000, Guangdong, Peoples R China
[3] Guangdong Med Univ, Affliated Hosp, Orthopaed Ctr, South Renmin Rd 57, Zhanjiang 524000, Guangdong, Peoples R China
关键词
Skeletal muscle atrophy; Myotubes; Cell models; MYOGENIC DIFFERENTIATION; UBIQUITIN-PROTEASOME; SIGNALING PATHWAY; DEXAMETHASONE; INFLAMMATION; EXPRESSION; AUTOPHAGY; IL-6; AMELIORATION; MECHANISMS;
D O I
10.1016/j.biopha.2023.115517
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
Skeletal muscle, the largest organ in the human body, plays a crucial role in supporting and defending the body and is essential for movement. It also participates in regulating the processes of protein synthesis and degradation. Inhibition of protein synthesis and activation of degradation metabolism can both lead to the development of skeletal muscle atrophy, a pathological condition characterized by a decrease in muscle mass and fiber size. Many physiological and pathological conditions can cause a decline in muscle mass, but the underlying mechanisms of its pathogenesis remain incompletely understood, and the selection of treatment strategies and efficacy evaluations vary. Moreover, the early symptoms of this condition are often not apparent, making it easily overlooked in clinical practice. Therefore, it is necessary to develop and use cell models to understand the eti-ology and influencing factors of skeletal muscle atrophy. In this review, we summarize the methods used to construct skeletal muscle cell models, including hormone, inflammation, cachexia, genetic engineering, drug, and physicochemical models. We also analyze, compare, and evaluate the various construction and assessment methods.
引用
收藏
页数:10
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