肾缺血再灌注致急性肾损伤肾素-血管紧张素系统的研究。

IF 4.1
Farzaneh Karimi, Maryam Maleki, Mehdi Nematbakhsh
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引用次数: 2

摘要

肾缺血再灌注损伤(RIRI)是一系列复杂的事件,定义为血供减少后再灌注。RIRI是急性肾损伤(AKI)的主要原因。在参与iri诱导AKI的多种介质中,肾素-血管紧张素系统(RAS)通过常规(血管紧张素原、肾素、血管紧张素转换酶(ACE)、血管紧张素(Ang) II和Ang II型1受体(AT1R))和非常规(ACE2、Ang 1-7、Ang 1-9、AT2受体(AT2R)和Mas受体(MasR))轴发挥重要作用。RIRI改变了两个轴的平衡,因此RAS可以影响RIRI诱导的AKI。总的来说,RIRI对Ang II/AT1R和AKI的改变是重要的考虑因素。这篇综述研究了在RIRI条件下RAS活性的影响和相互作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
View of the Renin-Angiotensin System in Acute Kidney Injury Induced by Renal Ischemia-Reperfusion Injury.
Renal ischemia-reperfusion injury (RIRI) is a sequence of complicated events that is defined as a reduction of the blood supply followed by reperfusion. RIRI is the leading cause of acute kidney injury (AKI). Among the diverse mediators that take part in RIRI-induced AKI, the renin-angiotensin system (RAS) plays an important role via conventional (angiotensinogen, renin, angiotensin-converting enzyme (ACE), angiotensin (Ang) II, and Ang II type 1 receptor (AT1R)) and nonconventional (ACE2, Ang 1-7, Ang 1-9, AT2 receptor (AT2R), and Mas receptor (MasR)) axes. RIRI alters the balance of both axes so that RAS can affect RIRI-induced AKI. In overall, the alteration of Ang II/AT1R and AKI by RIRI is important to consider. This review has looked for the effects and interactions of RAS activities during RIRI conditions.
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