摘要
铁自噬介导铁死亡在脓毒症及其相关器官功能障碍中具有调节作用。铁自噬通过特定载体核受体激活因子4(NCOA4)介导,将细胞内的铁蛋白转移到自噬溶酶体中进行降解并释放出游离铁,以满足多种铁依赖的生理过程需要。铁自噬是构成铁死亡机制的重要组成部分。本文综述铁自噬与铁死亡机制在脓毒症治疗中的研究进展,为深入了解其发病机制和脓毒症相关器官功能障碍提供新的治疗方向。
The recent studies have revealed the regulatory mechanism of ferritinophagy-mediated ferroptosis in sepsis and sepsis-associated organ dysfunction.The ferritinophagy,mediated by the specific carrier nuclear receptor coactivator 4(NCOA4),transfers intracellular iron proteins to autophagic lysosomes for degradation and release of free iron to meet the requirements of various iron-dependent physiological processes.The ferritinophagy is a crucial component of the ferroptosis mechanism.This article reviews the mechanisms of ferritinophagy and ferroptosis in research progress of the sepsis treatment,and provides new therapeutic directions for a deeper understanding of its pathogenesis and sepsis-related organ dysfunction.
作者
王勉
康印东
李佛荣
李家豪
蒋星明
常德辉
Wang Mian;Kang Yindong;Li Forong;Li Jiahao;Jiang Xingming;Chang Dehui(First School of Clinical Medical,Gansu University of Chinese Medicine,Lanzhou 730050,China)
出处
《中国急救医学》
CAS
CSCD
2024年第4期361-365,共5页
Chinese Journal of Critical Care Medicine
基金
甘肃省卫生健康行业科研基金(GSWSKY2020-71)
部队专项培育项目(2021yxky041)。
关键词
铁自噬
铁死亡
核受体共激活因子4
脓毒症
心肌损伤
急性肺损伤
急性肾损伤
Ferritinophagy
Ferroptosis
Nuclear receptor coactivator 4
Sepsis
Myocardial injury
Acute lung injury
Acute lung kidney injury
