炎症中的血管紧张素AT2受体。

Franziska Rompe, Thomas Unger, Ulrike Muscha Steckelings
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引用次数: 40

摘要

慢性炎症越来越被认为不仅是持续感染危险的结果,而且是许多非传染性疾病(如自身免疫性疾病、糖尿病或心血管疾病)的一个组成部分。因此,一些激素系统,如肾素-血管紧张素系统(RAS),最初是在心血管疾病的背景下被描述的,也被证明是炎症反应的主要调节者,这并不奇怪。本文综述了RAS在炎症中的作用,特别强调了血管紧张素AT(2)受体的作用。虽然血管紧张素AT(1)受体的促炎特性已被证实,但目前大多数证据支持AT(2)受体具有抗炎作用。然而,关于炎症中这种受体的数据仍然相当稀少,并且有些争议。本文将讨论AT(2)受体偶联干扰促炎途径的主要机制以及来自特定疾病动物模型的数据。最后,简要展望了AT(2)受体研究的新可能性,以及AT(2)受体刺激作为一种新的药理学概念在抗炎中的潜在应用。
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The angiotensin AT2 receptor in inflammation.

Chronic inflammation is increasingly regarded not just as a consequence of a continuous infectious hazard, but also as an integral part of many noninfectious diseases such as autoimmune disorders, diabetes or cardiovascular disease. Thus, it is not surprising that some hormonal systems, like the renin-angiotensin system (RAS), which were originally described in the context of cardiovascular disease have also turned out to be major regulators of the inflammatory response. This review focuses on the role of the RAS in inflammation, with particular emphasis on the role of the angiotensin AT(2) receptor. While the proinflammatory features of the angiotensin AT(1) receptor are well established, most current evidence supports an anti-inflammatory role for AT(2) receptor. However, data on this receptor in inflammation are still rather sparse and are somewhat controversial. This article will discuss the principal mechanisms of AT(2) receptor-coupled interference with proinflammatory pathways as well as data derived from animal models of specific diseases. Finally, it will give a brief outlook into new possibilities in AT(2) receptor research and in the potential utilization of AT(2) receptor stimulation as a novel pharmacological concept in anti-inflammation.

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来源期刊
Drug news & perspectives
Drug news & perspectives 医学-药学
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