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肾缺血/再灌注损伤:水通道蛋白的可能作用。

Renal ischaemia/reperfusion injury: possible role of aquaporins.

机构信息

Department of Physiology, Faculty of Medicine, Mansoura University, Egypt.

出版信息

Acta Physiol (Oxf). 2012 Mar;204(3):308-16. doi: 10.1111/j.1748-1716.2011.02372.x. Epub 2011 Nov 5.

Abstract

Renal ischaemia/reperfusion (I/R) injury is a common problem that occurs when blood flow is interrupted to the kidney in case of kidney transplantation, aortic cross-clamping and shock with subsequent resuscitation. Renal I/R injury is a complex conditions which includes the onset of an inflammatory process, which is associated with impairment of concentrating ability of the kidney and impairment of solute transport. Characteristically, renal I/R injury is associated with marked reduction in the protein expression of renal aquaporins (AQPs) mainly (AQP1, AQP2 and AQP3), and solute transporters were observed in this condition and could account for the impaired urinary concentration that observed in this condition. Recently, many agents were tested for a possible protective effect against this insult such as erythropoietin (EPO), α-melanocyte-stimulating hormone (α-MSH) and α-lipoic acid which were proved to prevent downregulation of AQPs and solute transporters. The aim of this short review is to outline the potential pathophysiological role of AQPs in renal I/R injury and to put a spotlight on the modulation of renal functions impairment in renal ischaemia by new drugs that prevent downregulation of AQPs.

摘要

肾缺血/再灌注(I/R)损伤是一种常见的问题,当肾脏血流中断时会发生这种情况,如肾移植、主动脉夹闭和休克后复苏。肾 I/R 损伤是一种复杂的情况,包括炎症过程的发生,这与肾脏浓缩能力的损害和溶质转运的损害有关。特征性地,肾 I/R 损伤与肾水通道蛋白(AQPs)的蛋白质表达显著减少有关,主要是(AQP1、AQP2 和 AQP3),并且在这种情况下观察到溶质转运体,这可以解释在这种情况下观察到的尿浓缩受损。最近,许多药物被测试是否具有对抗这种损伤的可能保护作用,如促红细胞生成素(EPO)、α-黑素细胞刺激素(α-MSH)和α-硫辛酸,这些药物被证明可以防止 AQPs 和溶质转运体的下调。本综述的目的是概述 AQPs 在肾 I/R 损伤中的潜在病理生理作用,并强调通过预防 AQPs 下调的新药来调节肾缺血时的肾功能损害。

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