脑缺血再灌注损伤中线粒体动力学的研究进展  

Research progress of mitochondrial dynamics in cerebral ischemia/reperfusion injury

作　　者：莫燕资 袁张莉 谢露[2] 陈蒙华[1,2] MO Yan-Zi;YUAN Zhang-Li;XIE Lu;CHEN Meng-Hua(Second Affiliated Hospital of Guangxi Medical University,Nanning 530007,China;Guangxi Medical University,Nanning 530021,China)

机构地区：[1]广西医科大学第二附属医院,南宁530007 [2]广西医科大学,南宁530021

出　　处：《生命科学》2022年第6期702-710,共9页Chinese Bulletin of Life Sciences

基　　金：国家自然科学基金项目(81860333);广西青年科学基金项目(2018GXNSFBA281045)。

摘　　要：脑缺血再灌注损伤的发生机制十分复杂,伴随着钙超载以及ROS生成爆发导致线粒体形态和功能异常。线粒体动力学(融合、分裂)是维持线粒体正常形态和功能的关键,该过程主要由线粒体融合蛋白和分裂蛋白调控。线粒体融合/分裂失衡与脑缺血再灌注损伤的发生发展密切相关,研究表明Ca^(2+)超载和ROS通过影响线粒体动力学蛋白而调控线粒体融合和分裂,决定神经元的存亡。该文就脑缺血再灌损伤中涉及的线粒体动力学相关分子及相关机制的研究作一综述,为临床上减轻脑损伤疾病提供新的思路。Cerebral ischemia/reperfusion injury occurs by complex mechanisms,with calcium overload and bursts of ROS production leading to abnormal mitochondrial morphology and function.Mitochondrial dynamics(fusion,fission)are critical for maintaining normal mitochondrial morphology and function,and the process is mainly regulated by mitochondrial fusion and fission proteins.Mitochondrial fusion/fission imbalance is closely related to the development of cerebral ischemia/reperfusion injury,and studies have shown that Ca^(2+)overload and ROS regulate mitochondrial fusion and fission by affecting mitochondrial kinetic proteins,which determine neuronal survival.This paper presents a review of studies involving molecules related to mitochondrial dynamics and related mechanisms in cerebral ischemia/reperfusion injury to provide new ideas for clinical mitigation of brain injury diseases.

关 键 词：线粒体动力学 脑缺血再灌注损伤 钙超载 活性氧 凋亡 自噬 

分 类 号：R741.02[医药卫生—神经病学与精神病学] R743.3[医药卫生—临床医学]