Abstract
Skeletal muscle dysfunction (SMD), one of the extrapulmonary complications in patients with chronic obstructive pulmonary disease (COPD), considerably influences patient prognosis. Mitochondria regulates their dynamic networks through a mitochondria quality control (MQC) mechanism, involving mitochondrial biogenesis, mitochondrial dynamics, and mitophagy. The MQC is crucial for mitochondrial homeostasis and health, and disruption of it can lead to mitochondrial damage, which is a key factor in the structural and functional impairment of skeletal muscle in COPD. The mitochondria in the skeletal muscles of these patients undergo changes, mainly including decrease in mitochondrial density and biogenesis levels, imbalanced mitochondrial fission and fusion, and altered mitophagy status. However, the potential mechanisms linking MQC to the damaged structure and function of skeletal muscles in COPD have not been fully clarified. Therefore, this review highlights the effects and potential pathways of the MQC system on the dysfunction of skeletal muscle (muscle atrophy, impaired myogenesis and regeneration, and aerobic endurance) in patients with COPD, and summarizes potential interventions targeted MQC, intending to provide a theoretical basis for further research on COPD, improve SMD, and enhance the quality of life.