去神经支配
萎缩
肌肉萎缩
肌节
骨骼肌
神经再支配
肌肉肥大
炎症
内科学
心肌细胞
内分泌学
解剖
化学
生物
细胞生物学
医学
作者
Maria Angels Rodríguez,Claudio Cabello‐Verrugio
出处
期刊:Current Protein & Peptide Science
[Bentham Science]
日期:2024-03-01
卷期号:25 (3): 189-199
标识
DOI:10.2174/0113892037189827231018092036
摘要
Abstract: Skeletal muscle tissue has the critical function of mechanical support protecting the body. In addition, its functions are strongly influenced by the balanced synthesis and degradation processes of structural and regulatory proteins. The inhibition of protein synthesis and/or the activation of catabolism generally determines a pathological state or condition called muscle atrophy, a reduction in muscle mass that results in partial or total loss of function. It has been established that many pathophysiological conditions can cause a decrease in muscle mass. Skeletal muscle innervation involves stable and functional neural interactions with muscles via neuromuscular junctions and is essential for maintaining normal muscle structure and function. Loss of motor innervation induces rapid skeletal muscle fiber degeneration with activation of atrophy-related signaling and subsequent disassembly of sarcomeres, altering normal muscle function. After denervation, an inflammation stage is characterized by the increased expression of pro-inflammatory cytokines that determine muscle atrophy. In this review, we highlighted the impact of some soluble factors on the development of muscle atrophy by denervation.
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