线粒体功能障碍与血管内皮损伤的研究进展  

The research progress on mitochondrial dysfunction and vascular endothelial cell injury

作　　者：闫明静 沈涛[1,2] YAN Mingjing;SHEN Tao(The Key Laboratory of Geriatrics,Beijing Institute of Geriatrics,Institute of Geriatric Medicine,Chinese Academy of Med-ical Sciences,Beijing Hospital/National Center of Gerontology of National Health Commission,Beijing 100730,China;Peking University Fifth School of Clinical Medicine,Beijing 100730,China)

机构地区：[1]北京医院国家老年医学中心国家卫生健康委北京老年医学研究所国家卫生健康委老年医学重点实验室中国医学科学院老年医学研究院 [2]北京大学第五临床医学院,北京市100730

出　　处：《中国动脉硬化杂志》2021年第10期829-837,共9页Chinese Journal of Arteriosclerosis

基　　金：国家自然科学基金项目(81770228、81470427)。

摘　　要：线粒体功能障碍会导致ATP的生成减少,活性氧的产生增加,被认为是血管内皮损伤的触发因素之一。许多因素与线粒体功能障碍有关,如线粒体DNA突变、线粒体融合与分裂失衡、线粒体自噬受损等。本文综述了线粒体的质量控制过程和线粒体功能障碍在血管内皮损伤中的作用机制,以期为动脉粥样硬化的有效防治提供新的思路。Mitochondrial dysfunction can lead to ATP decrease and reactive oxygen species increase in cells.Therefore,mitochondrial dysfunction is considered to be one of the culprit factors of vascular endothelial cell injury.Many causes are related to mitochondrial dysfunction including mitochondrial DNA mutations,mitochondrial fusion and fission imbalance,and mitophagy dysfunction.This review discussed the regulation mechanisms of mitochondrial quality control and mitochondrial dysfunction in vascular endothelial cell injury,which provide new ideas for the effective prevention and treatment of atherosclerosis.

关 键 词：内皮损伤 线粒体功能障碍 线粒体融合与分裂 线粒体自噬 线粒体DNA突变 

分 类 号：R5[医药卫生—内科学]