运动调节线粒体-内质网结构偶联缓解衰老性肌萎缩的研究进展

Role of mitochondrial-endoplasmic reticulum structural coupling in relief of sarcopenia induced by exercise

随着人口老龄化的加剧,衰老导致骨骼肌组织数量和质量退化,造成肌肉萎缩的发生率日趋增加,威胁着老年人的健康。衰老性肌萎缩(即肌肉减少症,sarcopenia)是一种慢性退行性疾病,主要表征为肌肉质量、力量和功能的下降,伴随摔倒、致残、发病和死亡率的增加[1],可能与线粒体功能障碍、内质网应激(endoplasmic reticulum stress, ERS)等反应有关[2-3]。预防衰老性肌萎缩将成为老年医学领域亟待解决的重要问题,运动作为一种经济有效的健康促进手段.

Exercise is an effective intervention to prevent muscle atrophy, and its mechanism may be related to improving the interaction between mitochondria and endoplasmic reticulum in the aging process. Mitochondria-endoplasmic reticulum coupling, also known as mitochondria-associated endoplasmic reticulum membranes(MAMs), is a subcellular structure connecting mitochondria and endoplasmic reticulum. The MAMs plays important roles in exerting the functions between mitochondria and endoplasmic reticulum. Here we reviewed the structure of MAMs, aging muscular atrophy and MAMs function, and the molecular targets of exercise-mediated MAMs in relieving aging muscular atrophy. The MAMs-related mechanisms by which exercise attenuates sarcopenia are determined by multiple factors such as Ca2+transfer, the balance of mitochondrial fusion and fission, oxidative stress, endoplasmic reticulum stress, activation of mitophagy, inflammation and apoptosis. This review may provide references for the treatment of sarcopenia.