氧化应激与NOD样/Toll样受体在急性肾损伤中的研究进展

Advances in oxidative stress and NOD-like/toll-like receptors in acute renal injury

急性肾损伤(acute kidney injury,AKI)是以快速肾功能恶化为特征的的临床综合征,发病率和死亡率高。肾脏再灌注损伤(renal reperfusion injury,IRI)占所有AKI病因的75%。IRI导致的AKI病死率高,且存活的患者存在不同程度的慢性肾功能损伤。目前多项研究表明导致肾脏功能异常的缺血再灌注损伤与氧化应激直接相关,且通过NOD样/Toll样受体信号传导通路抑制氧化应激产生,可减轻肾脏缺血再灌注损伤,本文就调节氧化应激及固有免疫受体与急性肾损伤关系的研究进展作一综述。

Acute Kidney Injury(AKI)is a clinical syndrome characterized by rapid renal deterioration with high morbidity and mortality.Renal reperfusion(IRI),renal toxicity and sepsis are the main causes of AKI.IRI is one of the main causes of acute kidney injury in clinic,accounting for 75%of all the causes of AKI.The fatality rate of AKI caused by IRI is high,and the surviving patients may leave chronic renal impairment with different degrees.A number of studies have shown that ischemia-reperfusion injury leading to renal dysfunction is directly related to oxidative stress,and the inhibition of oxidative stress through nod-like/toll-like signaling pathway can reduce acute renal injury.This review summarizes the research progress in regulating oxidative stress and the relationship between innate immune receptors and acute renal injury.