线粒体融合蛋白Mfn2在阿尔茨海默病中的研究进展

Progress of the mitochondrial fusion protein Mfn2 in Alzheimer's disease

线粒体融合蛋白2(Mfn2)作为调节线粒体融合的关键因子,通过调控线粒体的融合裂变过程来维持线粒体数量、结构和生物功能等动态变化,线粒体动力学的稳态是调节细胞器功能的前提,线粒体功能障碍是包括阿尔茨海默病(AD)在内的神经退行性疾病的特征之一。在AD患者的大脑中,β-淀粉样蛋白(Aβ)聚集和Tau蛋白过度磷酸化的同时,Mfn2的表达水平明显下降,因此,Mfn2在AD的发病过程中可能发挥重要的作用。本文主要综述了Mfn2在AD线粒体动力学中的作用。了解Mfn2与AD发病机制的相关性,将为开发与线粒体功能障碍相关疾病的治疗提供重要信息。

Mitofusion2(Mfn2),a key factor regulating mitochondrial fusion,maintains dynamic changes in mitochondrial number,structure and biological functions by modulating the fusion and fission processes of mitochondria.The homeostasis of mitochondrial dynamics is the premise of regulating organelle function.Mitochondrial dysfunction is one of the characteristics of neurodegenerative diseases,including Alzheimer's disease(AD).In the brains of AD patients,β-amyloid(Aβ)aggregation and hyperphosphorylation of Tau proteins are accompanied by a significant decrease in the expression level of Mfn2,suggesting Mfn2 may play an important role in the pathogenesis of AD.This review focuses on the role of Mfn2 in mitochondrial dynamics of AD.Understanding the correlation between Mfn2 and the pathogenesis of AD will provide important information for the development of the treatment of mitochondrial dysfunction-related diseases.