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失活骨骼肌中蛋白质合成的调控:信号输入、蛋白激酶级联反应和核糖体生物发生

Regulation of Protein Synthesis in Inactivated Skeletal Muscle: Signal Inputs, Protein Kinase Cascades, and Ribosome Biogenesis.

作者信息

Mirzoev T M, Shenkman B S

机构信息

Institute of Biomedical Problems, Russian Academy of Sciences, Moscow, 123007, Russia.

出版信息

Biochemistry (Mosc). 2018 Nov;83(11):1299-1317. doi: 10.1134/S0006297918110020.

Abstract

Disuse atrophy of skeletal muscles is characterized by a significant decrease in the mass and size of muscle fibers. Disuse atrophy develops as a result of prolonged reduction in the muscle functional activity caused by bed rest, limb immobilization, and real or simulated microgravity. Disuse atrophy is associated with the downregulation of protein biosynthesis and simultaneous activation of protein degradation. This review is focused on the key molecular mechanisms regulating the rate of protein synthesis in mammalian skeletal muscles during functional unloading.

摘要

骨骼肌的废用性萎缩表现为肌纤维的质量和大小显著下降。废用性萎缩是由于卧床休息、肢体固定以及实际或模拟微重力导致肌肉功能活动长期减少而产生的。废用性萎缩与蛋白质生物合成的下调以及蛋白质降解的同时激活有关。本综述聚焦于调节哺乳动物骨骼肌在功能卸载期间蛋白质合成速率的关键分子机制。

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