线粒体功能障碍参与动脉粥样硬化的分子机制  

Molecular Mechanisms of Mitochondrial Dysfunction Involved in Atherosclerosis

作　　者：司艳红[1,2] 陈晓凤[1] 秦树存[1] 

机构地区：[1]泰山医学院动脉粥样硬化研究所,山东省高校动脉粥样硬化重点实验室,山东泰安271000 [2]泰山医学院基础医学院,山东泰安271000

出　　处：《中国生物化学与分子生物学报》2015年第9期897-903,共7页Chinese Journal of Biochemistry and Molecular Biology

基　　金：山东省泰山学者岗专项基金资助项目(No.zd056;zd057);山东省高校科技计划项目(No.J09LF69)资助~~

摘　　要：以往认为,线粒体的主要功能是提供能量,目前发现线粒体还是调节细胞氧化应激与凋亡的关键部位,并且与毗邻的细胞器内质网保持密切联系.线粒体功能障碍时,可通过加重机体氧化应激、炎症反应、细胞凋亡及胆固醇蓄积等病理过程,影响动脉粥样硬化(AS)的发生发展.本综述首先简单介绍了线粒体的基本功能,然后重点分析线粒体功能障碍时,参与AS的最新证据及其分子机制.此方面研究提示,线粒体可能是AS的潜在治疗靶点.Mitochondria are often regarded as the cellular powerhouses through their ability to generate ATP. However,in recent years mitochondria have been recognised as critical site of regulating oxidative stress and apoptosis in cell. And it is closely related to endoplasmic reticulum which is adjacent to mitochondria. Mitochondrial dysfunction can promote oxidative stress,inflammation,cell apoptosis and cholesterol accumulation. These are key processes in atherosclerosis（ AS）. In this review, the fundamental function of mitochondria was first introduced. Then the latest evidences and their molecular mechanisms on the contribution of mitochondrial dysfunction to AS were discussed thoroughly. These studies indicated that mitochondria could be the potential therapeutic target for AS.

关 键 词：线粒体功能障碍 动脉粥样硬化 氧化应激 凋亡 

分 类 号：R589.2[医药卫生—内分泌]