自噬:运动改善神经退行性疾病的关键机制  

Autophagy:the critical mechanism of exercise in improving neurodegenerative diseases

作　　者：陈祥和[1] 仇啸 刘驰 沈梓铭 周香香 CHEN Xianghe;QIU Xiao;LIU Chi;SHEN Ziming;ZHOU Xiangxiang(College of Physical Education,Yangzhou University,Yangzhou 225127,China)

机构地区：[1]扬州大学体育学院,江苏扬州225127

出　　处：《中国比较医学杂志》2023年第10期132-139,共8页Chinese Journal of Comparative Medicine

基　　金：江苏省社会科学基金(20TYC001);中国博士后科学基金特别资助(2021T140580);中国博士后科学基金面上资助(2019M661957);扬州大学“高端人才支持计划”;扬州大学“青蓝工程”培养对象资助。

摘　　要：自噬调控神经类疾病是当前神经科学领域的研究焦点。自噬紊乱导致Aβ、Tau、α-syn等蛋白表达、沉积和功能失调,引发阿尔茨海默症、帕金森病、亨廷顿病等神经退行性疾病。运动是改善神经退行性疾病的重要手段,这与AdipoR1/AMPK/TFEB、AMPK/mTOR等途径被激活后上调LC3、Beclin-1、Lamp1等自噬因子表达密切相关,较高的自噬水平可清除脑中沉积的Aβ、Tau、α-syn等蛋白,改善神经退行性疾病引起的神经元变性、突触结构和功能紊乱等。本研究综述分析了自噬在运动改善神经退行性疾病中的作用机制,将为运动改善神经退行性疾病研究提供坚实的理论依据和新的研究思路。Autophagy regulation of neurological diseases is the focus of current research in the field of neuroscience.Autophagy disorder leads to expression,deposition,and dysfunction of proteins such as Aβ,Tau,α-syn,and causes neurodegenerative diseases such as Alzheimer’s disease,Parkinson’s disease and Huntington’s disease.Exercise is important to improve neurodegenerative diseases,which is closely related to upregulated expression of LC3,Beclin-1,Lamp1 and other autophagic factors after activation of AdipoR1/AMPK/TFEB,AMPK/mTOR,and other pathways.A high autophagy level removes deposition of Aβ,Tau,α-syn and other proteins in the brain and improves neurodegeneration and synaptic structure and function disorder caused by neurodegenerative diseases.This article reviewed and analyzed the mechanism of autophagy in the improvement of neurodegenerative diseases by exercise,which provides a solid theoretical basis and new research ideas to improve neurodegenerative diseases by exercise.

关 键 词：自噬 运动 神经退行性疾病 作用机制 

分 类 号：R-33[医药卫生]