线粒体功能障碍与肌少-骨质疏松症关联性研究进展
Progress in exploring the association between mitochondrial dysfunction and sarcopenia and osteoporosis
  
DOI:10.3969/j.issn.1006-7108.2026.08.020
中文关键词:  肌少症  骨质疏松症  线粒体功能障碍  线粒体能量代谢  氧化应激
英文关键词:sarcopenia  osteoporosis  mitochondrial dysfunction  mitochondrial energy metabolism  oxidative stress
基金项目:甘肃省高校产业支撑计划项目(2025CYZC-051);兰州市城关区人才创新创业项目(2023-rc-7);兰州市科技计划项目(2023-2-83)
作者单位
陆韵霖1 吴俊媛1 董万涛2* 方志杰1 1.甘肃中医药大学,甘肃 兰州 730000 2.甘肃中医药大学附属医院,甘肃 兰州 730000 
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中文摘要:
      肌少-骨质疏松症(osteosarcopenia,OS)是指肌肉减少症与骨质疏松症共存的疾病状态,是一种随年龄增长而出现的肌骨系统疾患。它显著降低了老年群体生活质量,大幅提升了跌倒、骨折、残疾乃至死亡的发生几率。OS致病因素错综复杂,而线粒体功能障碍在OS发生发展中起关键作用。线粒体功能障碍是指线粒体在结构、代谢或调控过程中出现异常,导致其无法正常执行生理功能的状态。其不仅影响能量代谢,还会引发氧化应激、电子传递链失衡、线粒体动力学异常、细胞死亡信号异常等连锁反应,最终导致细胞和组织损伤,甚至全身性病理改变。基于此,本文聚焦线粒体功能障碍,探讨其在OS发病机制中的作用,旨在为OS的临床治疗提供新思路,开辟新路径。
英文摘要:
      Osteosarcopenia (OS) refers to a disease state characterized by the coexistence of sarcopenia and osteoporosis, a musculoskeletal disorder that emerges with advancing age. It significantly diminishes the quality of life in elderly population and markedly increases the risks of falls, fractures, disability, and even mortality. The pathogenic factors of OS are complex, with mitochondrial dysfunction playing a pivotal role in its onset and progression. Mitochondrial dysfunction denotes an abnormal state where mitochondria fail to perform their physiological functions properly due to disruptions in structure, metabolism, or regulatory processes. This dysfunction not only impairs energy metabolism but also triggers a cascade of responses, including oxidative stress, electron transport chain imbalance, mitochondrial dynamics abnormalities, and dysregulated cell death signaling, ultimately leading to cellular and tissue damage, as well as systemic pathological changes. Against this backdrop, this paper focuses on mitochondrial dysfunction, exploring its role in the pathogenesis of OS, with the aim of providing novel insights and approaches for the clinical treatment of OS.
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