文章摘要
张珂玮,宋媛,赵莹,姚黎清,王寿梅,王敏佳.线粒体功能障碍在心衰后骨骼肌萎缩中的机制研究[J].中国康复,2026,41(5):297-302
线粒体功能障碍在心衰后骨骼肌萎缩中的机制研究
Mechanistic study of mitochondrial dysfunction in skeletal muscle atrophy following heart failure
  
DOI:10.3870/zgkf.2026.05.008
中文关键词: 线粒体  心力衰竭  骨骼肌萎缩
英文关键词: mitochondria  heart failure  skeletal muscle atrophy
基金项目:云南省重点研发计划(202203AC100007-6);云南省康复临床医学中心(zx2019-04-02)
作者单位
张珂玮 昆明医科大学第二附属医院康复医学部,昆明650106 
宋媛 浙江省人民医院毕节医院康复科 
赵莹 昆明医科大学第二附属医院康复医学部,昆明650106 
姚黎清 昆明医科大学第二附属医院康复医学部,昆明650106 
王寿梅 昆明医科大学第二附属医院康复医学部,昆明650106 
王敏佳 昆明医科大学第二附属医院康复医学部,昆明650106 
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中文摘要:
  在心衰所诱导的外周骨骼肌萎缩的有关机制中,线粒体功能障碍近年来备受关注。心衰患者骨骼肌中线粒体能量生成障碍、活性氧累积、钙稳态失衡、线粒体DNA突变、动力学失衡(融合/分裂异常)、线粒体自噬、细胞凋亡通路活化及线粒体生物合成减少等是导致心衰后肌纤维萎缩的关键机制,这些线粒体功能障碍在心衰后的骨骼肌萎缩中主要涉及两个方面,一是心力衰竭后导致的心脏问题进而导致骨骼肌功能障碍,二是心衰后由于失用、缺氧等因素致骨骼肌直接发生变化,这两个方面都会加剧肌肉代谢异常。但是目前尚有诸多不明确的机制需要探讨。本文综述了线粒体功能障碍与心衰后骨骼肌萎缩的联系,并针对线粒体功能障碍的不同类型对心衰后骨骼肌萎缩的影响进行探讨,以期为心衰患者的肌肉萎缩防治提供理论依据。
英文摘要:
  Mitochondrial dysfunction has gained considerable attention in recent years as a central contributor to peripheral skeletal muscle atrophy secondary to heart failure (HF). In skeletal muscle from patients with HF, impaired mitochondrial energy production, excessive accumulation of reactive oxygen species (ROS), disrupted calcium homeostasis, mitochondrial DNA (mtDNA) mutations, imbalanced mitochondrial dynamics (abnormal fusion and fission), dysregulated mitophagy, activation of apoptotic pathways, and reduced mitochondrial biogenesis have all been implicated as key mechanisms driving post-HF myofiber wasting. Broadly, the mitochondrial derangements that promote skeletal muscle atrophy after HF operate through two non-mutually exclusive pathways: cardiac impairment caused by HF that secondarily induces skeletal muscle dysfunction; direct alterations within skeletal muscle triggered by HF-associated factors such as disuse, hypoxia, and systemic metabolic disturbances. Both pathways exacerbate metabolic abnormalities in muscle. Nevertheless, important mechanistic uncertainties remain. This review summarizes current evidence linking mitochondrial dysfunction to skeletal muscle atrophy following HF and discusses how distinct dimensions of mitochondrial impairment influence the development and progression of muscle wasting, with the aim of providing a theoretical basis for strategies to prevent and treat muscle atrophy in patients with HF.
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