解读表达血红素加氧酶-1（HO-1）的巨噬细胞在肾脏缺血再灌注损伤中的作用
Deciphering the Role of Heme Oxygenase-1 (HO-1) Expressing Macrophages in Renal Ischemia-Reperfusion Injury.
作者信息
Rossi Maxime, Korpak Kéziah, Doerfler Arnaud, Zouaoui Boudjeltia Karim
机构信息
Department of Urology, CHU de Charleroi, Université libre de Bruxelles (ULB), 6000 Charleroi, Belgium.
Laboratory of Experimental Medicine (ULB 222 Unit), CHU de Charleroi, Hôpital André Vésale, Université libre de Bruxelles (ULB), 6110 Montigny-le-Tilleul, Belgium.
出版信息
Biomedicines. 2021 Mar 16;9(3):306. doi: 10.3390/biomedicines9030306.
Ischemia-reperfusion injury (IRI) is a leading cause of acute kidney injury (AKI), which contributes to the development of chronic kidney disease (CKD). Renal IRI combines major events, including a strong inflammatory immune response leading to extensive cell injuries, necrosis and late interstitial fibrosis. Macrophages act as key players in IRI-induced AKI by polarizing into proinflammatory M1 and anti-inflammatory M2 phenotypes. Compelling evidence exists that the stress-responsive enzyme, heme oxygenase-1 (HO-1), mediates protection against renal IRI and modulates macrophage polarization by enhancing a M2 subset. Hereafter, we review the dual effect of macrophages in the pathogenesis of IRI-induced AKI and discuss the critical role of HO-1 expressing macrophages.
缺血再灌注损伤（IRI）是急性肾损伤（AKI）的主要原因，而急性肾损伤会促使慢性肾脏病（CKD）的发展。肾脏IRI涉及多个主要事件，包括强烈的炎症免疫反应，进而导致广泛的细胞损伤、坏死以及后期的间质纤维化。巨噬细胞通过极化为促炎性M1和抗炎性M2表型，在IRI诱导的AKI中发挥关键作用。有确凿证据表明，应激反应酶血红素加氧酶-1（HO-1）可介导对肾脏IRI的保护作用，并通过增强M2亚群来调节巨噬细胞极化。在此，我们综述巨噬细胞在IRI诱导的AKI发病机制中的双重作用，并讨论表达HO-1的巨噬细胞的关键作用。
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