血红素加氧酶-1与肾脏损伤

Kidney injury and heme oxygenase-1

血红素加氧酶-1(HO-1)作为哺乳动物降解血红素的主要途径之一,其主要降解产物——一氧化碳(CO)、自由铁(Fe2+)和胆绿素——在促进细胞生存、细胞内物质循环及免疫调节中具有重要作用。既往研究提示血红素-HO-1通路是决定急性肾损伤(AKI)易感性及严重性的重要内在因素。诱导HO-1表达能够减轻肾脏缺血-再灌注损伤(IRI)的严重程度,而抑制HO-1的表达会加重IRI。本文综述了国内外有关HO-1在AKI诱导保护机制方面的最新研究进展,以便深入认识HO-1在AKI治疗中的作用。

Heme oxygenase-1 （HO-1） is one of the main pathways to degrade heme in mammals, and the main degradation products are free iron （Fe2＋）, carbon monoxide （CO）, and bilirubin. Heine plays an important role in promoting cell survival, circulation of intracellular substrates, and immune regulation. Previous studies suggest that the heme-HO-1 pathway is an important internal factor in determining the susceptibility and severity of acute kidney injury （AKI）. The induction of HO-1 expression can attenuate the severity of renal ischemia-reperfusion injury （IRI）, and the inhibition of riO-1 expression will accentuate the injury of IRI. The present article summarizes the latest advances in research into HO-1 regarding the protective mechanism on AKI conducted abroad and at home to learn more information about HO-1 in the treatment of AKI.