Autophagy in skeletal muscle dysfunction of chronic obstructive pulmonary disease: implications, mechanisms, and perspectives.

Xiaoyu HAN; Peijun LI; Meiling JIANG; Yuanyuan CAO; Yingqi WANG; Linhong JIANG; Xiaodan LIU; Weibing WU

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Autophagy in skeletal muscle dysfunction of chronic obstructive pulmonary disease: implications, mechanisms, and perspectives.

Author: Xiaoyu HAN ¹ ; Peijun LI ² ; Meiling JIANG ¹ ; Yuanyuan CAO ¹ ; Yingqi WANG ² ; Linhong JIANG ² ; Xiaodan LIU ^{3
,

4} ; Weibing WU ^{4
,

5}
Author Information

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. School of Rehabilitation Science, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China. hzhp403@
4. com.
5. Department of Sports Rehabilitation, Shanghai University of Sport, Shanghai 200438, China. wwb75@
Publication Type:Review
Keywords: Autophagy; Chronic obstructive pulmonary disease; Mitochondria; Muscle satellite cell; Skeletal muscle dysfunction
MeSH: Pulmonary Disease, Chronic Obstructive/physiopathology*; Autophagy/physiology*; Humans; Muscle, Skeletal/pathology*; Mitophagy; Animals; Mitochondria/metabolism*; Lysosomes
From: Journal of Zhejiang University. Science. B 2025;26(3):227-239
CountryChina
Language:English
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.