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The role of macrophage polarization and interaction with renal tubular epithelial cells in ischemia-reperfusion induced acute kidney injury

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Author:: No author available

Journal Title:: Acta Physiologica Sinica

Issue:: 1

DOI:: 10.13294/j.aps.2022.0006

Key Word:: 急性肾损伤;促红细胞生成素受体;外泌体;缺血再灌注;巨噬细胞;备解素;肾小管上皮细胞

Abstract：急性肾损伤(acute kidney injury,AKI)是以肾功能急剧衰退为主要表现的常见危重临床疾病.缺血再灌注(ischemia-reperfusion,IR)是AKI的主要病因之一.由于缺乏早期诊断方法和针对病因的特异性治疗,AKI的死亡率一直居高不下.IR快速诱发固有免疫反应,激活补体和固有免疫细胞,释放大量损伤相关分子如高迁移率族蛋白B1(high mobility group box-1,HMGB1)、趋化因子及炎症介质如caspase-3,进而募集免疫炎症细胞如M1型巨噬细胞(Mφ)至肾损伤微环境中,引起肾小管上皮细胞(tubular epithelial cells,TECs)坏死和凋亡.死亡细胞及相关炎症进一步激活适应性免疫系统,在加重组织损伤的同时,也启动了M2型Mφ参与的炎症清除、组织再生及修复的程序.职业吞噬细胞Mφ和半职业化吞噬细胞TECs协同吞噬周围的损伤细胞,包括凋亡的Mφ及TECs,是调节损伤、修复或纤维化转归的关键固有免疫细胞.近年来研究发现促红细胞生成素(erythropoietin,EPO)不仅与同源二聚受体(EPOR)2结合诱导红细胞生成,还与异源二聚受体(EPOR/βcR),亦称固有修复受体(innate repair receptor,IRR),结合而发挥组织保护作用.备解素(properdin)是补体旁路激活过程中唯一的正性调节因子,能有效识别并结合早期凋亡T细胞,协助其通过非补体激活依赖机制被Mφ清除.我们课题组的前期研究表明Mφ、TECs、EPO及其受体和备解素等关联,参与IR损伤和修复,但其确切机制需要进一步研究.外泌体作为细胞间信号传递的重要载体,参与多种肾脏疾病的发生及发展,但其在IR诱导AKI的过程中如何影响Mφ和TECs间互动尚未完全明确.本文根据已有关于Mφ和TECs在肾IR所致AKI中作用的研究结果,进一步讨论Mφ极化、与TECs互动以及EPO、备解素及外泌体在其中的作用.

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