转录因子EB调控自噬溶酶体通路减轻脑缺血后神经元损伤  

Transcription factor EB attenuates neuronal damage following cerebral ischemia via regulating autophagy-lysosomal pathway

作　　者：李丹[1] 左夏林[1] 徐恩[1] Li Dan;Zuo Xialin;Xu En(Institute of Neurosciences,Department of Neurology,the Second Affiliated Hospital of Guangzhou Medical University,Guangzhou 510260,China)

机构地区：[1]广州医科大学神经科学研究所,广州医科大学附属第二医院神经内科,广州510260

出　　处：《国际脑血管病杂志》2023年第4期308-311,共4页International Journal of Cerebrovascular Diseases

基　　金：国家自然科学基金(81971233);广州市科技计划项目(202102010056)。

摘　　要：自噬溶酶体途径(autophagy-lysosomal pathway,ALP)紊乱是脑缺血后神经元损伤的重要发病机制,而恢复ALP有可能减轻脑缺血后神经元损伤。作为调节ALP的主要转录因子,转录因子EB(transcription factor EB,TFEB)可调控自噬基因和溶酶体基因表达,直接调节自噬体生成、自噬体溶酶体融合和自噬通量。因此,通过调控TFEB能够缓解ALP功能障碍,进而减轻脑缺血损伤。文章对TFEB的结构、生物学功能及其调控ALP减轻脑缺血后神经元损伤的作用进行了综述。The disorder of autophagy lysosomal pathway(ALP)is an important pathogenesis of neuronal damage after cerebral ischemia,and the restoration of ALP may alleviate neuronal damage after cerebral ischemia.As the main transcription factor regulating ALP,transcription factor EB(TFEB)can directly regulate autophagosome generation,autophagosome-lysosome fusion,and autophagic flux by regulating the expression of autophagic genes and lysosomal genes.Therefore,regulating TFEB can alleviate ALP dysfunction and thereby reduce cerebral ischemic damage.This article reviews the structure,biological function of TFEB and its role in regulating ALP to alleviate neuronal damage after cerebral ischemia.

关 键 词：脑缺血 碱性螺旋-环-螺旋亮氨酸拉链转录因子 自噬 溶酶体 神经保护药 信号转导 

分 类 号：R743.3[医药卫生—神经病学与精神病学]