骨骼肌废用性萎缩信号通路及蛋白质代谢的研究进展  

Research advance on signaling pathways and protein metabolism for skeletal muscle disuse atrophy

作　　者：李高权[1] 刘雪云[1] 徐守宇[1,2] 

机构地区：[1]浙江中医药大学附属第三医院,浙江杭州310005 [2]日本顺天堂大学医学部

出　　处：《中国骨伤》2013年第11期969-972,共4页China Journal of Orthopaedics and Traumatology

基　　金：浙江省省自然科学基金项目(编号LY12H17003);国家中医药管理局重点学科建设项目(国中医药人教发〔2012〕32号)~~

摘　　要：骨骼肌废用性萎缩是临床常见问题,其机制尚未完全明确。既往研究认为废用性萎缩的发生是通过一条或多条细胞信号通路的激活来实现,但也有研究指出废用性萎缩是泛素-蛋白酶体的活化而导致蛋白大量分解的结果。目前对于废用性萎缩的研究主要集中在NF-κB、IGF-1/PI3K/Akt、TGF-β/Smad及MAPK信号通路对上游信号分子MuRF1和Atroginl/MAFbx的调控作用以及多条信号通路激活或抑制及其相互作用,进而通过泛素-蛋白酶体来影响蛋白质代谢。但对于MuRF1和Atroginl/MAFbx表达的调控机制还有待研究,参与废用性萎缩基因的确认和功能验证也需要深入研究。Disuse atrophy of skeletal muscle is a common clinical problem and its exact mechanisms have not been fully understood. Previous studies suggested that disuse muscle atrophy is realized through the activation of one or more cell signaling pathways, but studies have shown that disuse atrophy is the activation of the ubiquitin-proteasome caused extensive decomposition of the protein. The present researches for disuse atrophy mainly focus on regulatory role in the upstream signaling molecules MuRF1 and Atroginl/MAFbx by NF-KB, IGF-1/PI3K/Akt, TGF-β/Smad and MAPK signal pathway and a plural- ity of signal pathway activation or inhibition and interaction,and then through the ubiquitin- proteasome to influence the metabolism of protein. But regulation of expression of MuRF1 and Atroginl/MAFbxs still to be studied. Participate in disuse at- rophy also needs to be further studied with atrophy confirmation and functional gene verification. The paper summarized recent original articles about the researches of skeletal muscle disuse atrophy and reviewed the various signal pathways and related ubiquitin-proteasome protein metabolism of disuse muscle atrophy.

关 键 词：肌 骨骼 肌萎缩 综述文献 

分 类 号：R730.5[医药卫生—肿瘤]