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运动靶向自噬机制治疗肌肉减少症。

Sarcopenia targeting with autophagy mechanism by exercise.

机构信息

Aging Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon 34141; Department of Life Science, University of Science and Technology (UST), Daejeon 34113, Korea.

Aging Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon 34141, Korea.

出版信息

BMB Rep. 2019 Jan;52(1):64-69. doi: 10.5483/BMBRep.2019.52.1.292.

Abstract

The loss of skeletal muscle, called sarcopenia, is an inevitable event during the aging process, and significantly impacts quality of life. Autophagy is known to reduce muscle atrophy caused by dysfunctional organelles, even though the molecular mechanism remains unclear. Here, we have discuss the current understanding of exercise-induced autophagy activation in skeletal muscle regeneration and remodeling, leading to sarcopenia intervention. With aging, dysregulation of autophagy flux inhibits lysosomal storage processes involved in muscle biogenesis. AMPK-ULK1 and the FoxO/PGC-1ɑ signaling pathways play a critical role in the induction of autophagy machinery in skeletal muscle, thus these pathways could be targets for therapeutics development. Autophagy has been also shown to be a critical regulator of stem cell fate, which determines satellite cell differentiation into muscle fiber, thereby increasing muscle mass. This review aims to provide a comprehensive understanding of the physiological role of autophagy in skeletal muscle aging and sarcopenia. [BMB Reports 2019; 52(1): 64-69].

摘要

骨骼肌的丧失,称为肌肉减少症,是衰老过程中不可避免的事件,极大地影响了生活质量。自噬被认为可以减少由功能失调的细胞器引起的肌肉萎缩,尽管其分子机制尚不清楚。在这里,我们讨论了运动诱导的自噬在骨骼肌再生和重塑中的激活作用,从而导致肌肉减少症的干预。随着年龄的增长,自噬通量的失调抑制了参与肌肉发生的溶酶体储存过程。AMPK-ULK1 和 FoxO/PGC-1α 信号通路在骨骼肌中自噬机制的诱导中起着关键作用,因此这些通路可能是治疗开发的靶点。自噬也被证明是干细胞命运的关键调节剂,它决定了卫星细胞分化为肌纤维,从而增加肌肉质量。本综述旨在全面了解自噬在骨骼肌衰老和肌肉减少症中的生理作用。[BMB 报告 2019;52(1):64-69]。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c74/6386226/1cb4f8d94e7f/bmb-52-064f1.jpg

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