Regulation of muscle hypertrophy: Involvement of the Akt-independent pathway and satellite cells in muscle hypertrophy
Regulation of muscle hypertrophy: Involvement of the Akt-independent pathway and satellite cells in muscle hypertrophy
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DOI：
10.1016/j.yexcr.2021.112907
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发表时间：
2021-11-19
影响因子：
3.7
通讯作者：
Ito, Naoki
中科院分区：
文献类型：
--
作者：
Fukada, So-ichiro;Ito, Naoki
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。为了响应由身体活动引起的机械负荷，骨骼肌发挥几种局部适应，包括肌纤维尺寸和肌纤维数量的增加，称为肌肉肥大。蛋白质合成和肌肉卫星细胞（MuSC）主要负责这些适应。然而，促进蛋白质合成的上游信号通路仍然存在争议。此外，MuSC在肌肉肥大中的必要性也是一个备受争议的问题。本文综述了非胰岛素样生长因子1（IGF-1）/Akt依赖性激活哺乳动物雷帕霉素靶蛋白（mTOR）信号通路在肌肉肥大中的作用，以及mTOR信号通路在年龄相关性骨骼肌功能和质量损失以及肌肉减少症中的作用。本文对MuSC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相关性进行了综述。
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.