Clinical Research Laboratory, Department of Biochemistry, Maharshi Dayanand University, Rohtak-124001, Haryana, India.
Division of Biochemistry, Indian Agricultural Research Institute, New Delhi, 110012, India.
Curr Med Chem. 2021;28(28):5831-5846. doi: 10.2174/0929867328666210202113734.
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失控的炎症和氧化应激状态，会导致蛋白质分解代谢加剧。最近的研究进展表明，肌纤维中 Toll 样受体（TLR）控制的信号分子受到影响。已确定激活的 TLR 信号通路是肌肉质量的抑制剂，并引发肌肉萎缩的发生。其中，TLR2 和 TLR4 主要表现出它们的存在，以加剧促炎细胞因子的释放，从而破坏肌肉的同步编程。本综述阐明了 TLR 信号介导的肌肉丢失以及炎症和骨骼肌肉生长之间的相互作用。
