线粒体蛋白质稳态在运动延缓和改善阿尔茨海默病中的作用与机制研究进展

Research Progress on the Role and Mechanism of Mitochondrial Proteostasis in Exercise Delay and Improvement of Alzheimer’s Disease

梳理运动通过调节线粒体蛋白质稳态从而预防和改善阿尔茨海默病(Alzheimer’s disease,AD)的研究进展与机制。近年研究发现:AD患者脑内线粒体蛋白质稳态失衡,引发线粒体功能紊乱;运动能够调节脑内线粒体蛋白质稳态,但具体机制尚不明确。运动可能通过4条途径调节线粒体蛋白质稳态进而预防和改善AD:1)激活线粒体未折叠蛋白反应;2)提高线粒体自噬进而清除受损的线粒体;3)调节线粒体蛋白质转运,调控线粒体蛋白质水平;4)改善线粒体氧化磷酸化,调节机体的能量代谢以及降低氧化应激。

Reviewing the research progress and mechanism of exercise in preventing and improving Alzheimer’s disease(AD) by regulating mitochondrial proteostasis. In recent years, it has been found that the imbalance of mitochondrial proteostasis in the brain of AD patients which leading to mitochondrial dysfunction;appropriate exercise can regulate mitochondrial proteostasis in brain, but the specific mechanism is not clear. Exercise may regulate mitochondrial proteostasis to prevent and improve AD through four pathways: 1) Activating mitochondrial unfolded protein response;2) increasing mitochondrial autophagy to remove damaged mitochondria;3) regulating mitochondrial protein transport and regulating mitochondrial protein level;4)improving mitochondrial oxidative phosphorylation, regulating energy metabolism and reducing oxidative stress.