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New Cardiovascular and Pulmonary Therapeutic Strategies Based on the Angiotensin-Converting Enzyme 2/Angiotensin-(1–7)/Mas Receptor Axis

机译:基于血管紧张素转换酶2 /血管紧张素-(1-7)/ Mas受体轴的新的心血管和肺治疗策略

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Angiotensin (Ang)-(1–7) is now recognized as a biologically active component of the renin-angiotensin system (RAS). The discovery of the angiotensin-converting enzyme homologue ACE2 revealed important metabolic pathways involved in the Ang-(1–7) synthesis. This enzyme can form Ang-(1–7) from Ang II or less efficiently through hydrolysis of Ang I to Ang-(1–9) with subsequent Ang-(1–7) formation. Additionally, it is well established that the G protein-coupled receptor Mas is a functional ligand site for Ang-(1–7). The axis formed by ACE2/Ang-(1–7)/Mas represents an endogenous counter regulatory pathway within the RAS whose actions are opposite to the vasoconstrictor/proliferative arm of the RAS constituted by ACE/Ang II/AT1receptor. In this review we will discuss recent findings concerning the biological role of the ACE2/Ang-(1–7)/Mas arm in the cardiovascular and pulmonary system. Also, we will highlight the initiatives to develop potential therapeutic strategies based on this axis.
机译:血管紧张素(Ang)-(1-7)现在被认为是肾素-血管紧张素系统(RAS)的生物活性成分。血管紧张素转换酶同系物ACE2的发现揭示了参与Ang-(1-7)合成的重要代谢途径。该酶可以从Ang II形成Ang-(1-7),或者通过将Ang I水解为Ang-(1-9)并随后形成Ang-(1-7)的效率较低。此外,公认的是,G蛋白偶联受体Mas是Ang-(1-7)的功能性配体位点。 ACE2 / Ang-(1-7)/ Mas形成的轴代表RAS中的内源性反调节途径,其作用与ACE / Ang II / AT1受体构成的RAS的血管收缩/增殖臂相反。在这篇综述中,我们将讨论有关ACE2 / Ang-(1-7)/ Mas臂在心血管和肺系统中的生物学作用的最新发现。此外,我们将重点介绍基于此轴开发潜在治疗策略的举措。

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