线粒体自噬相关受体蛋白和信号通路在运动防治肌少症中的作用

The role of mitochondrial autophagy-related receptor proteins and signaling pathways in the prevention and treatment of sarcopenia through exercise

背景:肌少症是一种衰老相关的退行性综合征,线粒体自噬和运动防治肌少症已被证明密切相关,但尚缺乏详细介绍其中具体的受体蛋白和信号通路在运动防治肌少症中作用的综述。目的:综述详细介绍线粒体自噬相关具体的受体蛋白和信号通路在运动防治肌少症中的作用。方法:在2023-02-01/04-01之间进行了文献检索,检索文献时限从各数据库建库至2023年4月,数据库包括Web of Science、PubMed、中国知网、万方和维普。涵盖了“肌少症,衰老,老年,线粒体,线粒体功能,蛋白,通路”等关键词,严格按照纳入和排除标准进行筛选,最终纳入文献76篇进行综述分析。结果与结论:①肌少症是随着年龄增长肌肉质量和功能下降的疾病,其发生机制涉及神经肌肉功能下降、慢性炎症、酸碱失衡和线粒体功能障碍等。②线粒体自噬是细胞清除受损线粒体的重要过程,其中相关受体蛋白以及信号通路参与线粒体自噬的调控,运动可以通过调节这些受体蛋白和信号通路的活性,促进线粒体自噬的发生,对防治肌少症具有重要作用。③运动通过调控多个通路来促进线粒体自噬,包括上调AMPK、磷酸化ULK1、降低线粒体能量、增加与AMBRA1相关蛋白的表达、调控PINK1/Parkin通路等,从而改善肌少症引发的线粒体功能障碍;此外,运动还能激活mTOR通路促进肌肉生长和增加对葡萄糖的摄取,预防和治疗肌少症。④未来需要进一步深入研究运动防治肌少症中线粒体自噬相关受体蛋白和信号通路的具体作用机制和调控途径,开展更多的人体临床研究,以推动该领域的进一步发展。

BACKGROUND:Sarcopenia is an age-related degenerative syndrome,and the relationship between mitochondrial autophagy and exercise in preventing and treating sarcopenia has been demonstrated.However,there is a lack of comprehensive reviews detailing the specific receptor proteins and signaling pathways involved in the role of exercise in sarcopenia prevention and treatment.OBJECTIVE:To comprehensively introduce the specific receptor proteins and signaling pathways related to mitochondrial autophagy and their role in the prevention and treatment of sarcopenia through exercise.METHODS:A literature search was conducted between February 1,2023,and April 1,2023,covering literature from database inception to April 2023.Keywords used for the search criteria,76 articles were ultimately included.RESULTS AND CONCLUSION:Sarcopenia is a disease characterized by a decline in muscle mass and function with age,and its pathogenesis involves neuro-muscular functional decline,chronic inflammation,acid-base imbalance,and mitochondrial dysfunction.Mitochondrial autophagy is an important process for clearing damaged mitochondria in cells,in which receptor proteins and signaling pathways are involved in the regulation of mitochondrial autophagy.Exercise can promote the occurrence of mitochondrial autophagy by regulating the activity of these receptor proteins and signaling pathways,thereby playing an important role in the prevention and treatment of sarcopenia.Exercise can induce mitochondrial autophagy in sarcopenia by upregulating AMPK,phosphorylating ULK1,and reducing mitochondrial energy,enhancing the expression of mitochondrial autophagy-related proteins associated with AMBRA1,and regulating the PINK1/Parkin pathway,to improve mitochondrial dysfunction caused by sarcopenia.In addition,exercise can activate the mTOR pathway to promote muscle growth and increase glucose uptake,thereby preventing and treating sarcopenia.Future studies are needed to further investigate the specific mechanisms and regulatory pathways of mitochondrial autophagy-related receptor proteins and signaling pathways in the prevention and treatment of sarcopenia by exercise,and to conduct more clinical trials in humans,thereby to promote further development in this field.