自噬在慢性阻塞性肺疾病骨骼肌功能障碍中的作用、机制和展望

韩晓雨; 李培君; 姜美玲; 曹媛媛; 王颖祺; 姜林鸿; 刘晓丹; 吴卫兵

doi:10.1631/jzus.B2300680

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自噬在慢性阻塞性肺疾病骨骼肌功能障碍中的作用、机制和展望

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Review | Updated：2025-03-13

自噬在慢性阻塞性肺疾病骨骼肌功能障碍中的作用、机制和展望
Autophagy in skeletal muscle dysfunction of chronic obstructive pulmonary disease: implications, mechanisms, and perspectives
浙江大学学报（英文版）（B辑：生物医学和生物技术） 2025年26卷第3期页码：227-239
Affiliations：

1.Department of Sports Rehabilitation, Shanghai University of Sport, Shanghai 200438, China
2.School of Rehabilitation Science, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China
3.Institute of Rehabilitation Medicine, Shanghai Academy of Traditional Chinese Medicine, Shanghai 201203, China
4.Engineering Research Center of Traditional Chinese Medicine Intelligent Rehabilitation, Ministry of Education, Shanghai 201203, China
Funds：

the National Natural Science Foundation of China(82172551);the Health Discipline Leader Project of Shanghai Municipal Health Commission(2022XD044)
DOI：10.1631/jzus.B2300680
中图分类号：
CSTR：
收稿日期：2023-09-19，

修回日期：2023-12-22，

网络出版日期：2025-03-01，

纸质出版日期：2025-03-13
Accepted：

韩晓雨,李培君,姜美玲等.自噬在慢性阻塞性肺疾病骨骼肌功能障碍中的作用、机制和展望[J].浙江大学学报（英文版）（B辑：生物医学和生物技术）,2025,26(03):227-239.

Xiaoyu HAN, Peijun LI, Meiling JIANG, et al. Autophagy in skeletal muscle dysfunction of chronic obstructive pulmonary disease: implications, mechanisms, and perspectives[J]. Journal of zhejiang university-science b (biomedicine & biotechnology), 2025, 26(3): 227-239.
韩晓雨,李培君,姜美玲等.自噬在慢性阻塞性肺疾病骨骼肌功能障碍中的作用、机制和展望[J].浙江大学学报（英文版）（B辑：生物医学和生物技术）,2025,26(03):227-239. DOI： 10.1631/jzus.B2300680.

Xiaoyu HAN, Peijun LI, Meiling JIANG, et al. Autophagy in skeletal muscle dysfunction of chronic obstructive pulmonary disease: implications, mechanisms, and perspectives[J]. Journal of zhejiang university-science b (biomedicine & biotechnology), 2025, 26(3): 227-239. DOI： 10.1631/jzus.B2300680.

摘要

骨骼肌功能障碍是慢性阻塞性肺疾病（COPD）患者常见的肺外共病，与患者生活质量和存活率相关。自噬溶酶体途径作为机体蛋白水解系统，影响骨骼肌结构和功能。然而，促进和抑制自噬均被发现可显著改善COPD骨骼肌的结构和功能，但其中机制尚未可知。本文首先综述巨自噬和线粒体自噬对COPD骨骼肌结构和功能的作用，并进一步探究自噬介导COPD骨骼肌功能障碍的机制。结果表明，巨自噬和线粒体自噬相关蛋白在COPD骨骼肌中显著升高，促进巨自噬可显著提高COPD肌卫星细胞的肌生成和复制能力，而体外抑制COPD肌管巨自噬可增加肌管直径。线粒体自噬有助于通过清除COPD受损线粒体来维持线粒体稳态。综上，自噬作为改善COPD骨骼肌功能障碍的潜在靶点，仍需进一步研究其在调节COPD骨骼肌功能的具体机制，以加深对该领域的理解。

Abstract

Skeletal muscle dysfunction is a common extrapulmonary comorbidity of chronic obstructive pulmonary disease (COPD) and is associated with decreased quality-of-life and survival in patients. The autophagy lysosome pathway is one of the proteolytic systems that significantly affect skeletal muscle structure and function. Intriguingly

both promoting and inhibiting autophagy have been observed to improve COPD skeletal muscle dysfunction

yet the mechanism is unclear. This paper first reviewed the effects of macroautophagy and mitophagy on the structure and function of skeletal muscle in COPD

and then explored the mechanism of autophagy mediating the dysfunction of skeletal muscle in COPD. The results showed that macroautophagy- and mitophagy-related proteins were significantly increased in COPD skeletal muscle. Promoting macroautophagy in COPD improves myogenesis and replication capacity of muscle satellite cells

while inhibiting macroautophagy in COPD myotubes increases their diameters. Mitophagy helps to maintain mitochondrial homeostasis by removing impaired mitochondria in COPD. Autophagy is a promising target for improving COPD skeletal muscle dysfunction

and further research should be conducted to elucidate the specific mechanisms by which autophagy mediates COPD skeletal muscle dysfunction

with the aim of enhancing our understanding in this field.

关键词

Keywords

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