线粒体功能障碍在慢性阻塞性肺疾病合并肌少症中的研究进展
Research progress of mitochondrial dysfunction in chronic obstructive pulmonary disease complicated with sarcopenia
  
DOI:10.3969/j.issn.1006-7108.2026.10.018
中文关键词:  慢性阻塞性肺疾病  肌少症  线粒体功能障碍  线粒体自噬  线粒体动力学
英文关键词:chronic obstructive pulmonary disease  sarcopenia  mitochondrial dysfunction  mitophagy  mitochondrial dynamics
基金项目:安徽省高等学校科学研究项目(自然科学类)重点项目(2024AH051552)
作者单位
田羽佳1 徐大林2* 1.合肥科技职业学院,安徽 合肥 231201 2.安徽省庐江县人民医院,安徽 合肥 231501 
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中文摘要:
      肌少症以持续性骨骼肌质量与功能降低为特征,是慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)常见的全身性并发症。骨骼肌线粒体功能障碍是COPD肌少症的核心病理机制,其中线粒体生物发生降低、动力学异常、自噬受损、氧化应激等异常状态与骨骼肌合成、分解的稳态失衡密切相关。运动训练、营养补充、药物及活性成分、肌肉电刺激等手段被证实可通过增加骨骼肌线粒体密度、减轻氧化应激、调节线粒体动力学失衡等机制改善COPD肌少症,但靶向线粒体功能障碍的药物仍待开发,现有中药复方、天然活性成分等成分仍须临床验证其疗效及安全性,未来须深入探究靶向线粒体功能障碍的治疗策略,为COPD肌少症提供更多新的干预手段。
英文摘要:
      Sarcopenia, characterized by persistent decrease of skeletal muscle mass and function, is a common systemic complication of chronic obstructive pulmonary disease (COPD). Skeletal muscle mitochondrial dysfunction is the core pathological mechanism of COPD sarcopenia, in which abnormal conditions such as decreased mitochondrial biogenesis, abnormal dynamics, autophagy damage, and oxidative stress are closely related to the steady imbalance of skeletal muscle synthesis and decomposition. Exercise training, nutrition supplement, drugs and active ingredients, muscle electrical stimulation, and other means have been proved to relieve COPD sarcopenia by increasing the mitochondrial density of skeletal muscle, reducing oxidative stress, regulating mitochondrial dynamic imbalance, and other mechanisms. However, drugs targeting mitochondrial dysfunction still need to be developed. The existing Chinese medicine compound and natural active ingredients still need to be clinically verified for their efficacy and safety. In the future, it is necessary to explore the treatment strategies targeting mitochondrial dysfunction in order to provide more new intervention measures for COPD sarcopenia.
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