铁死亡在急性呼吸窘迫综合征作用机制中的研究进展  

Research progress on the mechanism of ferroptosis in acute respiratory distress syndrome

作　　者：冯帮海 梅鸿[2] 覃松[2] 陈淼[2] Bang-hai Feng;Hong Mei;Song Qin;Miao Chen(Department of Critical Care Medicine,Zunyi Hospital of Traditional Chinese Medicine,Zunyi,Guizhou,563000,China;Department of Critical Care Medicine(The Second Ward),Affiliated Hospital of Zunyi Medical University,Zunyi Guizhou,563000,China)

机构地区：[1]遵义市中医院重症医学科,贵州遵义563000 [2]遵义医学院附属医院重症医学科二病区,贵州遵义563000

出　　处：《中国现代医学杂志》2022年第13期63-68,共6页China Journal of Modern Medicine

基　　金：国家自然科学基金(No:81960362)。

摘　　要：铁死亡是一种由铁介导的磷脂过氧化与氧化应激驱动,与细胞凋亡、自噬和坏死有明显区别的新型程序性细胞死亡方式。其主要特征是二价铁离子介导的芬顿反应导致胞膜脂质过氧化,以及胱氨酸/谷氨酸反向转运体障碍引起的谷胱甘肽过氧化物酶4失活。目前研究发现,铁死亡与急性呼吸窘迫综合征的病理生理密切相关。该文综述铁死亡及其在急性呼吸窘迫综合征作用机制中的研究进展,以引起研究者对铁死亡在急性呼吸窘迫综合征中作用的关注。Ferroptosis is a new type of programmed cell death that is driven by iron-mediated phospholipid peroxidation and oxidative stress, which is distinct from apoptosis, autophagy, and necrosis. Its main feature is ferric iron-mediated Fenton reaction leading to membrane lipid peroxidation and cystine/glutamate antiporter(System Xc-) disorder-induced glutathione peroxidase 4(GPX4) inactivated. The current studies have found that ferroptosis is closely related to the pathophysiology of acute respiratory distress syndrome(ARDS). This article reviews the research progress of ferroptosis and its role in ARDS to draw researchers’ attention to the role of ferroptosis in ARDS.

关 键 词：铁死亡 急性呼吸窘迫综合征 脂质过氧化 急性肺损伤 氧化应激 

分 类 号：R563[医药卫生—呼吸系统]