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.

骨骼肌萎缩的特征是一种不受控制的炎症和氧化应激状态，会加剧蛋白质分解代谢。最近的进展支持通过 toll 样受体 (TLR) 控制的肌肉纤维中的撞击信号分子。激活的 TLR 信号通路已被确定为肌肉质量的抑制剂并引发肌肉萎缩。其中，主要是TLR2和TLR4的存在，加剧了促炎细胞因子的释放，使同步的肌肉程序发生变形。本综述阐明了 TLR 信号介导的肌肉损失以及炎症与骨骼肌生长之间的相互作用。