Yu Yonghui, Chu Wanli, Chai Jiake, Li Xiao, Liu Lingying, Ma Li
Burn and Plastic Surgery Department, The First Affiliated Hospital to People's Liberation Army General Hospital, Beijing 100048, P.R. China.
Mol Med Rep. 2016 Feb;13(2):1470-4. doi: 10.3892/mmr.2015.4748. Epub 2015 Dec 30.
Skeletal muscle atrophy, a conventional clinical feature in patients with cancer, chronic obstructive pulmonary disease, sepsis and severe burns, is defined as a reduction in muscle mass. During atrophy, the protein degradation is abnormally activated and the aberrance between protein synthesis and protein degradation results in muscle atrophy. Previous studies have demonstrated that miRNAs, small non-coding RNA molecules, serve an important role in the regulation of muscle atrophy. Further studies have indicated the implications of the ubiquitin-proteasome and PI3K/Akt/FoxO signaling pathways and myogenic regulatory factors in miRNA-mediated muscle atrophy. Therefore, in this review, the effects and molecular mechanisms of miRNAs on muscle atrophy are summarized, leading to the suggestion that miRNAs may serve as potential therapeutic targets in muscle atrophy.
骨骼肌萎缩是癌症、慢性阻塞性肺疾病、脓毒症和严重烧伤患者的常见临床特征,其定义为肌肉质量减少。在萎缩过程中,蛋白质降解被异常激活,蛋白质合成与蛋白质降解之间的失衡导致肌肉萎缩。先前的研究表明,微小RNA(miRNA),即小的非编码RNA分子,在肌肉萎缩的调节中起重要作用。进一步的研究表明泛素-蛋白酶体和PI3K/Akt/FoxO信号通路以及生肌调节因子在miRNA介导的肌肉萎缩中具有重要意义。因此,在本综述中,总结了miRNA对肌肉萎缩的影响及其分子机制,提示miRNA可能成为肌肉萎缩潜在的治疗靶点。