Cellular mechanisms regulating protein synthesis and skeletal muscle hypertrophy in animals

被引:136
作者
Miyazaki, Mitsunori [1 ]
Esser, Karyn A. [1 ]
机构
[1] Univ Kentucky, Coll Med, Dept Physiol, Lexington, KY 40536 USA
基金
美国国家卫生研究院;
关键词
mechanical stretch; REDD2; overload; IGF-1; amino acids; WORK-INDUCED GROWTH; P70; S6; KINASE; INTRACELLULAR SIGNALING SPECIFICITY; TUMOR-SUPPRESSOR COMPLEX; AMINO-ACID SUFFICIENCY; MAMMALIAN TARGET; RESISTANCE EXERCISE; GENE-EXPRESSION; PHOSPHATIDIC-ACID; TRANSGENIC MICE;
D O I
10.1152/japplphysiol.91355.2008
中图分类号
Q4 [生理学];
学科分类号
071003 [生理学];
摘要
Miyazaki M, Esser KA. Cellular mechanisms regulating protein synthesis and skeletal muscle hypertrophy in animals. J Appl Physiol 106: 1367-1373, 2009; doi:10.1152/japplphysiol.91355.2008.-Growth and maintenance of skeletal muscle mass is critical for long-term health and quality of life. Skeletal muscle is a highly adaptable tissue with well-known sensitivities to environmental cues such as growth factors, cytokines, nutrients, and mechanical loading. All of these factors act at the level of the cell and signal through pathways that lead to changes in phenotype through multiple mechanisms. In this review, we discuss the animal and cell culture models used and the signaling mechanisms identified in understanding regulation of protein synthesis in response to mechanical loading/resistance exercise. Particular emphasis has been placed on 1) alterations in mechanical loading and regulation of protein synthesis in both in vivo animal studies and in vitro cell culture studies and 2) upstream mediators regulating mammalian target of rapamycin signaling and protein synthesis during skeletal muscle hypertrophy.
引用
收藏
页码:1367 / 1373
页数:7
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