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肌肉肥大的调节: Akt 非依赖性途径和卫星细胞在肌肉肥大中的作用。

Regulation of muscle hypertrophy: Involvement of the Akt-independent pathway and satellite cells in muscle hypertrophy.

机构信息

Project for Muscle Stem Cell Biology, Graduate School of Pharmaceutical Sciences, Osaka University, Osaka, Japan.

Laboratory of Molecular Life Science, Institute of Biomedical Research and Innovation (IBRI), Foundation for Biomedical Research and Innovation at Kobe (FBRI), Kobe, Japan.

出版信息

Exp Cell Res. 2021 Dec 15;409(2):112907. doi: 10.1016/j.yexcr.2021.112907. Epub 2021 Nov 15.

DOI:10.1016/j.yexcr.2021.112907
PMID:34793776
Abstract

Skeletal muscles are composed of multinuclear cells called myofibers and have unique abilities, one of which is plasticity. In response to the mechanical load induced by physical activity, skeletal muscle exerts several local adaptations, including an increase in myofiber size and myonuclear number, known as muscle hypertrophy. Protein synthesis and muscle satellite cells (MuSCs) are mainly responsible for these adaptations. However, the upstream signaling pathways that promote protein synthesis remain controversial. Further, the necessity of MuSCs in muscle hypertrophy is also a highly debated issue. In this review, we summarized the insulin-like growth factor 1 (IGF-1)/Akt-independent activation of mammalian target of rapamycin (mTOR) signaling in muscle hypertrophy and the involvement of mTOR signaling in age-related loss of skeletal muscle function and mass and in sarcopenia. The roles and behaviors of MuSCs, characteristics of new myonuclei in muscle hypertrophy, and their relevance to sarcopenia have also been updated in this review.

摘要

骨骼肌由称为肌纤维的多核细胞组成,具有独特的能力,其中之一是可塑性。骨骼肌对体力活动引起的机械负荷会产生几种局部适应性,包括肌纤维大小和肌核数量的增加,即肌肉肥大。蛋白质合成和肌肉卫星细胞(MuSCs)主要负责这些适应性变化。然而,促进蛋白质合成的上游信号通路仍存在争议。此外,MuSCs 在肌肉肥大中的必要性也是一个备受争议的问题。在这篇综述中,我们总结了胰岛素样生长因子 1(IGF-1)/Akt 非依赖性雷帕霉素靶蛋白(mTOR)信号在肌肉肥大中的激活,以及 mTOR 信号在与年龄相关的骨骼肌功能和质量丧失以及肌肉减少症中的作用。在这篇综述中还更新了 MuSCs 的作用和行为、肌肉肥大中新肌核的特征及其与肌肉减少症的关系。

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