摘要
阿尔茨海默症(Alzheimer’s diseases,AD)是一种常见的神经退行性疾病,俗称老年性痴呆。脑内Aβ过度聚集、Tau蛋白过度磷酸化和神经元凋亡是AD的主要病理特征。小泛素样修饰蛋白(small ubiquitin-like modifier,SUMO)通过与底物蛋白结合参与蛋白质翻译后修饰,已被发现可通过以下方式参与AD的病理过程,主要有:(1)SUMO修饰BACE1,促进Aβ产生;(2)SUMO修饰Tau蛋白,促进其磷酸化并抑制其被泛素蛋白酶系统降解;(3)AD脑内SUMO化异常导致神经元过度凋亡。运动已被证实可改善AD病理特征,调节体内SUMO化水平,这提示运动缓解AD可能存在SUMO化机制。现通过综述SUMO与AD,以及运动对SUMO的影响,阐述SUMO介导的运动抗AD的可能机制。
Alzheimer’s disease(AD)is a neurodegenerative disease commonly known as dementia,characterized by excessive aggregation of Aβ,hyperphosphorylation of Tau protein and neuronal apoptosis.The small ubiquitinlike modifier(SUMO)is mainly involved in post-translational modification of proteins via binding to the substrate protein.And SUMO proteins are involved in the pathological process of AD in the following ways:(1)SUMO modifies BACE1,promoting Aβsecretion;(2)SUMO modifies Tau,enhancing its phosphorylation and inhibiting its degradation by ubiquitin protease system;(3)aberrant level of SUMOylation in AD leads to excessive neuron apoptosis.In addition,it has widely been demonstrated that exercise can mitigate the symptom of AD and regulate the level of SUMOylation in vivo,which infers to that there may be a SUMOylation mechanism in exerciserelieving AD.Therefore,this article reviews the mechanism of SUMOylation in AD and the effect of exercise on SUMO,aiming to expound the possible mechanism of SUMO-mediated exercise-relieving AD.
作者
张晨斐
赵娜
夏杰
王璟
徐波
ZHANG Chen-Fei;ZHAO Na;XIA Jie;WANG Jing;XU Bo(Key Laboratory of Aolescent Health Assessment and Exercise Interventin,Ministry of Enducation,East China Normal University,Shanghai 200241,China;College of Physical Education and Health,East China Normal University,Shanghai 200241,China)
出处
《生命科学》
CSCD
北大核心
2019年第11期1106-1115,共10页
Chinese Bulletin of Life Sciences
基金
国家自然科学基金项目(31571225)