肌肉生长抑制素对骨骼肌作用研究进展  被引量:8

Progress on Effects of Myostatin on Skeletal Muscle

在线阅读下载全文

作  者:杨惠[1] 额尔敦木图[1] 姜建强[1] 包花尔[1] 那仁巴图[2] 刘图雅 

机构地区:[1]内蒙古农业大学兽医学院农业部动物疾病临床诊疗技术重点实验室,内蒙古呼和浩特010018 [2]内蒙古农业大学动物科学学院,内蒙古呼和浩特010018 [3]内蒙古阿拉善左旗农牧业局兽医局,内蒙古巴彦浩特750300

出  处:《动物医学进展》2016年第5期77-82,共6页Progress In Veterinary Medicine

基  金:内蒙古自治区科技计划资助项目(201502069)

摘  要:肌肉生长抑制素(MSTN)是转化生长因子β超家族的成员之一,又称生长分化因子8。MSTN主要在骨骼肌中广泛表达,并可在心肌、脂肪、乳腺等多个组织中表达,其作用主要体现在抑制骨骼肌生长发育、诱发肌萎缩等方面。MSTN可以通过多种途径协同作用于骨骼肌,即通过激活TGF-β、p38MAPK、ERK1/2、JNK等信号途径以及抑制IGF-AKT、Wnt信号途径来抑制肌细胞增殖分化;通过调控AKT途径、泛素-蛋白水解酶系统、自噬溶酶体系统来影响骨骼肌蛋白的合成与分解;MSTN还参与了与骨骼肌生成相关的脂肪代谢及骨形成等生理活动。论文重点阐述MSTN在肌细胞增殖分化、肌蛋白合成与分解、脂肪代谢、骨骼发育等方面的作用机制,并对其应用前景进行展望,为相关科学研究提供参考。Myostatin(MSTN), also known as growth differentiation factor 8 (GDF-8), is a member oI transforming growth factor beta (TGF-beta) super family. MSTN is mainly expressed in skeletal muscle as well as other tissues including cardiac muscle, fat, breast, and plays significant roles in inhibiting growth and development of skeletal muscle and inducing muscle atrophy. Recent studies have shown that MSTN may act synergistically on skeletal muscle in different ways. MSTN inhibits proliferation and differentiation of muscle cells by activating TGF-beta, p38MAPK, ERK1/2, and JNK signaling pathways and IGF-AKT and Wnt signaling pathways,influences synthesis and decomposition of skeletal muscle protein by negative regulation of AKT pathway and regulation of the ubiquitin protease activity and autoph- agy-lysosome system. MSTN also participates in fat metabolism and physiological activities, such as bone formation, related to the generation of skeletal muscle. In this paper, starting with the signaling pathways MSTN acts on, we reviewed the effects of MSTN on proliferation and differentiation of muscle cells, synthesis and decomposition of muscle protein, fat metabolism, and skeletal development, and also summarized the application prespects of MSTN in order to provide references for further studies.

关 键 词:肌肉生长抑制素 骨骼肌 肌细胞 作用机制 

分 类 号:S852.2[农业科学—基础兽医学]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象