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Anti-inflammatory properties of drugs acting on the renin-angiotensin system.

机译:作用于肾素-血管紧张素系统的药物的抗炎特性。

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摘要

It is now well established that the activation of the renin-angiotensin system (RAS) is involved in the onset and progression of cardiovascular and renal diseases, and that its main effector, angiotensin II (Ang II) has major pro-inflammatory activity that induces the expression of cytokines, chemokines, adhesion molecules, growth factors and reactive oxygen species. By means of these actions, Ang II induces vascular inflammation, endothelial dysfunction and fibrosis, and participates in destabilizing atherosclerotic plaque and establishing chronic kidney diseases. Blocking the RAS by inhibiting Ang II generation or blocking angiotensin receptors reduces the morbidity and mortality associated with cardiovascular and renal disease beyond the levels due to the lowering of blood pressure, and these benefits are at least partially due to the reduction/prevention of both local and systemic inflammatory processes. The aim of this review is to describe the role of the RAS (and particularly Ang II) in initiating and maintaining these processes, and to summarize experimental and clinical evidence supporting the role of drugs acting on the RAS in preventing or modulating inflammation.
机译:现已确定,肾素-血管紧张素系统(RAS)的激活与心血管疾病和肾脏疾病的发作和发展有关,其主要效应物血管紧张素II(Ang II)具有主要的促炎活性,可诱导细胞因子,趋化因子,粘附分子,生长因子和活性氧的表达。通过这些作用,Ang II引起血管炎症,内皮功能障碍和纤维化,并参与破坏动脉粥样硬化斑块的稳定性和建立慢性肾脏疾病。通过抑制Ang II的产生来阻断RAS或阻断血管紧张素受体可以将与心血管和肾脏疾病相关的发病率和死亡率降低到超过由于血压降低而引起的水平,并且这些益处至少部分是由于降低/预防了两种局部和全身性炎症过程。这篇综述的目的是描述RAS(特别是Ang II)在启动和维持这些过程中的作用,并总结实验和临床证据,以支持作用于RAS的药物在预防或调节炎症中的作用。

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