摘要
脑卒中已成为中国成人致死和致残的首要原因.脑缺血后通过氧自由基增加、炎症反应、钙超载、能量代谢障碍等多种病理生理途径致细胞内稳态失衡,引起线粒体功能障碍,最终导致细胞死亡.线粒体生物发生(MB)通过产生新的功能性线粒体替换受损线粒体,恢复线粒体功能,是维持线粒体内稳态的主要机制,在线粒体质量控制方面发挥重要作用.近年来随着对缺血性脑卒中损伤机制研究的深入,线粒体生物发生被认为是一种具有潜在治疗效果的新靶点.本文就线粒体生物发生在脑缺血性损伤过程中作用和机制的研究进展进行综述,为缺血性脑卒中的神经保护治疗提供理论参考.
Abstract
Ischemic stroke has become the leading cause of mortality and disability among adults in China.After ce-rebral ischemia,various pathological and physiological pathways,including the increase in oxygen free radicals,inflam-matory response,calcium overload,and energy metabolism disorders,can disrupt cellular homeostasis,cause mitochon-drial dysfunction,and finally lead to cell apoptosis.By generating new functional mitochondria to replace damaged ones and restoring mitochondrial function,mitochondrial biogenesis(MB)is the primary mechanism for maintaining mitochon-drial homeostasis and plays a crucial role in mitochondrial quality control.In recent years,with the in-depth research on the mechanisms of ischemic stroke injury,MB has emerged as a potential therapeutic target.This article reviews the re-search advances in the role and mechanisms of MB in cerebral ischemic injury,in order to provide a theoretical reference for neuroprotective treatment in ischemic stroke.
基金项目
吉林省自然科学基金项目(自由探索重点项目)(YDZJ202401444ZYTS)
吉林省卫生科研人才专项项目(2023SCZ72)
维普
万方数据