Kelch-like ech-associated protein 1/nuclear factor E2-related factor 2/antioxidant response element pathway alleviates ferroptosis in sepsis by regulating oxidative stress
10.3760/cma.j.cn121430-20210130-00180
- VernacularTitle:Keap1/Nrf2/ARE信号通路可通过调节氧化应激缓解脓毒症过程中的细胞铁死亡
- Author:
Jiarou LI
1
;
Hongliang WANG
Author Information
1. 哈尔滨医科大学附属第二医院重症医学科，黑龙江哈尔滨 150086
- Keywords:
Nuclear factor E2-related factor 2;
Sepsis;
Oxidative stress;
Ferroptosis
- From:
Chinese Critical Care Medicine
2021;33(7):881-884
- CountryChina
- Language:Chinese
-
Abstract:
Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection, and has a high morbidity and mortality worldwide. The characteristic of sepsis is the inflammatory reaction. Cytokines produced by the severe inflammatory reaction can activate neutrophils and cause excessive production of reactive oxygen species (ROS), thus damage cells and tissue, and further develop into organ dysfunction and failure. Ferroptosis is an iron-dependent form of nonapoptotic cell death discovered recently. Its main mechanism is the intracellular lipid peroxidation induced by iron and the low expression of antioxidant systems [glutathione (GSH) and glutathione peroxidase 4 (GPX4)]. Recently, many studies have shown that Kelch-like ech-associated protein 1/nuclear factor E2-related factor 2/antioxidant response element (Keap1/Nrf2/ARE) signal pathway can improve oxidative stress and alleviate ferroptosis in sepsis. This article reviews the molecular mechanism and research of Nrf2 inhibiting ferroptosis in sepsis, in order to innovate prevention and treatments for the intervention of sepsis.
