缺血缺氧导致心肌自噬的分子机制  

The Molecular Mechanism of Myocardial Autophagy Induced by Ischemia and Hypoxia

作　　者：李兴岳 郭润民[1] 梁伟钧[1] 

机构地区：[1]广东医学院附属医院,广东湛江524000

出　　处：《中国医学创新》2015年第36期153-156,共4页Medical Innovation of China

基　　金：广东省科技计划项目(20110316)

摘　　要：自噬是自噬是细胞维持内环境稳态的重要方式之一,在各种生命活动中扮演着十分重要的角色。在能量缺乏或者缺血缺氧的情况下,通过自噬能够提供能量的中间产物以及降解异常的细胞器以维持细胞的正常生理活动。适当的自噬保护了在缺血缺氧情况下的细胞。本文在缺血缺氧情况下导致的心肌自噬的分子机制作一综述。Autophagy is one of the important ways to maintain cellular homeostasis and plays a very important role all kinds of life activities. In the absence of energy or in the case of ischemia and hypoxia, It would maintain the normal physiological activity of the ceils via autophagy which can provide the intermediate product for the energy and degrade the abnormal cells. Appropriate autophagy protects cells in the condition of ischemia and hypoxia. In this article, we summarize the molecular mechanism of myocardial autophagy caused by ischemia and hypoxia.

关 键 词：自噬 缺血 缺氧 心肌细胞 分子机制 

分 类 号：R329.2[医药卫生—人体解剖和组织胚胎学]