线粒体生物发生在脑缺血再灌注损伤中作用的研究进展  

Research Progress on the Mechanism of Mitochondrial Biogenesis in Cerebral Ischemia-Reperfusion Injury

作　　者：李晶晶 李瑞青[2] 张建云[1] 张帅迪 黄梦玲 李欣然 黄金 金小琴 Li Jingjing;Li Ruiqing;Zhang Jianyun(School of Rehabilitation,Henan University of Chinese Medicine,Zhengzhou 450046,China;Rehabilitation Center,the First Affiliated Hospital of Henan University of Chinese Medicine,Zhengzhou 450000,China)

机构地区：[1]河南中医药大学康复医学院,郑州450046 [2]河南中医药大学第一附属医院康复中心,郑州450000

出　　处：《华中科技大学学报(医学版)》2025年第2期298-304,共7页Acta Medicinae Universitatis Scientiae et Technologiae Huazhong

基　　金：河南省重点研发与推广专项(科技攻关)基金资助(No.232102310470);河南省科技研发计划联合基金(优势学科培育类)资助项目(No.222301420066);河南省中医药科学研究专项课题(No.2023ZXZX1163,No.2019JDZX2111)。

摘　　要：缺血性脑卒中(ischemic stroke,IS)是指脑血管突然受阻或闭塞而引起的急性脑血管疾病,是中国致残和死亡的主要原因之一。其主要治疗目标是在症状出现后尽快恢复血流,常采用静脉溶栓和血管内血栓切除术,但是溶栓后血液再通易导致脑缺血再灌注损伤(cerebral ischemia-reperfusion injury,CIRI)。CIRI是IS的关键病理过程,因此寻找减轻CIRI的方法至关重要。线粒体生物发生(mitochondrial biogenesis,MB)是指从现有线粒体协调合成新的线粒体。当脑缺血发生时,机体通过激活MB维持机体线粒体稳态,减轻氧化应激和炎症反应,使机体免受进一步的损伤。了解MB的分子机制及其激活路径可望为治疗CIRI提供新方向。该文总结了MB的分子机制,MB通过维持线粒体稳态、抑制IS后的氧化应激和炎症反应对CIRI产生保护的机制,以及激活MB改善CIRI的潜在治疗手段,以期为临床治疗CIRI提供新的思路。Ischemic stroke(IS)is an acute cerebrovascular disease caused by sudden obstruction or occlusion of cerebral blood vessels,and is one of the major causes of disability and death in China.The main therapeutic goal is to restore blood flow as soon as possible after the onset of symptoms,and intravenous thrombolysis and endovascular thrombectomy are often adopted.However,post-thrombolysis blood recirculation is prone to lead to cerebral ischemia-reperfusion injury(CIRI).CIRI is a key pathological process in IS,so it is critical to find ways to mitigate CIRI.Mitochondrial biogenesis(MB)coordinates synthesis of new mitochondria from existing ones.When cerebral ischemia occurs,the body maintains mitochondrial homeostasis by activating MB,alleviates oxidative stress and inflammatory response,and prevents the body from further damage.Understanding the molecular mechanism of MB and its activation pathway will provide a new direction for the treatment of CIRI.This review summarizes the molecular mechanism of MB,the protective mechanism of MB for CIRI by maintaining mitochondrial homeostasis,inhibiting oxidative stress and inflammation after IS,and the potential therapeutic targets to improve CIRI by activating MB.It will provide new ideas for clinical treatment of CIRI.

关 键 词：脑缺血再灌注损伤 线粒体生物发生 缺血性脑卒中 PGC-1Α SIRT1 

分 类 号：R743.3[医药卫生—神经病学与精神病学]