骨骼肌
炎症
肌肉萎缩
TLR4型
萎缩
TLR2型
受体
信号转导
细胞因子
细胞生物学
Toll样受体
内分泌学
生物
化学
内科学
免疫学
医学
先天免疫系统
作者
Aarti Yadav,Anil Dahuja,Rajesh Dabur
标识
DOI:10.2174/0929867328666210202113734
摘要
Skeletal muscle atrophy has been characterized as a state of uncontrolled inflammation and oxidative stress that escalates protein catabolism. Recent advancement supports impinging signaling molecules in the muscle fibers controlled through toll-like receptors (TLR). Activated TLR signaling pathways have been identified as inhibitors of muscle mass and provoke the settings for muscle atrophy. Among them, mainly TLR2 and TLR4 manifest their presence to exacerbate the release of the pro-inflammatory cytokine to deform the synchronized muscle programming. The present review enlightens the TLR signaling mediated muscle loss and the interplay between inflammation and skeletal muscle growth.
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