Peng Jianping, Chen Xiaodong
Department of Orthopedics, Affiliated Xinhua Hospital of the Medical School of Shanghai Jiaotong University, Shanghai 200092, PR China.
Zhongguo Xiu Fu Chong Jian Wai Ke Za Zhi. 2008 Dec;22(12):1511-4.
To summarize the recent progress in research on the mechanism of denervated skeletal muscle atrophy.
The recently-published literatures at home and abroad on denervated skeletal muscle atrophy were reviewed and summarized.
The mechanism of denervated skeletal muscle atrophy was very complex. At present, the study of the mechanism was based on the changes in histology, cytology and molecules. Fiber thinning and disorderly arrangement of denervated skeletal muscles were observed and apoptotic bodies were detected. Apoptosis-promoting genes expressed upregulatedly and apoptosis-restraining genes expressed down-regulatedly. Muscle satellite cells increased after denervation, but then they decreased and disappeared because they could not differentiate to mature muscle fibers. The structural change of cytomiscrosome and down-regulation of metabolism-related enzymes induced cell metabolism disorder.
The histological change of skeletal muscle fibers, the change of the number of muscle satellite cells and differentiation, the structural change of cytomiscrosome and the change of apoptosis-related and metabolism-related gene expressions contribute to denervated skeletal muscle atrophy.
总结失神经支配骨骼肌萎缩机制的研究进展。
查阅并总结国内外近期发表的关于失神经支配骨骼肌萎缩的文献。
失神经支配骨骼肌萎缩的机制非常复杂。目前，该机制的研究基于组织学、细胞学和分子水平的变化。观察到失神经支配骨骼肌纤维变细且排列紊乱，并检测到凋亡小体。促凋亡基因表达上调，抑凋亡基因表达下调。失神经支配后肌肉卫星细胞增多，但随后因无法分化为成熟肌纤维而减少并消失。细胞微粒体结构改变及代谢相关酶下调导致细胞代谢紊乱。
骨骼肌纤维的组织学变化、肌肉卫星细胞数量及分化的改变、细胞微粒体结构变化以及凋亡相关和代谢相关基因表达的变化导致失神经支配骨骼肌萎缩。
