自噬在急性肺损伤/急性呼吸窘迫综合征作用机制中的研究进展  

Research progress on autophagic mechanism in acute lung injury/acute respiratory distress syndrome

作　　者：冯帮海 刘国跃[1] 覃松[1] 陈涛[1] 陈淼[1] Feng Banghai;Liu Guoyue;Qin Song;Chen Tao;Chen Miao(Department of Critical Care Medicine (the Second Ward),Affiliated Hospital of Zunyi Medical University,Zunyi 563000,Guizhou,China)

机构地区：[1]遵义医学院附属医院重症医学科二病区,贵州遵义563000

出　　处：《中国中西医结合急救杂志》2019年第2期242-246,共5页Chinese Journal of Integrated Traditional and Western Medicine in Intensive and Critical Care

基　　金：国家自然科学基金(8156010205).

摘　　要：自噬是一种基本的细胞过程,其在亚细胞器和蛋白质的转换中起作用。激活自噬可阻止氧化应激导致的蛋白质受损或细胞器损伤的病理进展。选择性自噬通过降解受损的蛋白质维持细胞器的更新。现就自噬在急性肺损伤/急性呼吸窘迫综合征(ALI/ARDS)中的作用机制研究进展综述如下,从而加深对自噬的理解,引起研究者对自噬在ALI/ARDS中肺保护作用的关注。Autophagy is a fundamental cellular process that plays a role in the turnover of suh-cellular organelles to protein. The activation of autophagy may prevent the pathophysilogical progression of oxidative stressinduced protein damage or organelle damage. The selective form of autophagy can maintain organelle renewal by degrading damaged proteins. In this article, the research progress on the mechanism of autophagy in acute lung injury/ acute respiratory distress syndrome (ALI/ARDS) was summarized in order to understand more deeply on this topic and arouse more researchers to pay attention to the role of autophagy in lung protection of ALI/ARDS.

关 键 词：自噬 急性肺损伤 急性呼吸窘迫综合征 氧化应激 线粒体 

分 类 号：R563.8[医药卫生—呼吸系统]