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[心血管和肾脏疾病中的ACE2/血管紧张素(1-7)/Mas受体轴]

[The ACE2/Ang(1-7)/Mas receptor axis in cardiovascular and renal diseases].

作者信息

Kanda Takeshi, Itoh Hiroshi

机构信息

Health Center, School of Medicine, Keio University.

出版信息

Nihon Rinsho. 2012 Sep;70(9):1487-91.

PMID:23012792
Abstract

The renin-angiotensin-aldosterone system(RAAS) plays a crucial role in the regulation of physiological homeostasis and diseases such as hypertension, coronary artery disease and chronic renal failure. In this cascade, the ACE/Ang II/AT1 receptor axis induces pathological effects, such as vasoconstriction, cell proliferation and fibrosis. Recently the ACE2/Ang(1-7)/Mas receptor axis has been recognized as a negative regulator of the RAAS. ACE2 metabolizes Ang II into Ang(1-7), which has opposite properties of Ang II through Mas receptor activation. Both animal and human studies provide strong evidence that the ACE2/Ang(1-7)/Mas receptor axis is protective for end-organ damage. Therefore, the ACE2/Ang(1-7)/Mas receptor axis could be a therapeutic target for coronary artery disease and chronic renal failure.

摘要

肾素-血管紧张素-醛固酮系统(RAAS)在生理稳态调节以及高血压、冠状动脉疾病和慢性肾衰竭等疾病中发挥着关键作用。在这一连锁反应中,ACE/Ang II/AT1受体轴会引发诸如血管收缩、细胞增殖和纤维化等病理效应。最近,ACE2/Ang(1-7)/Mas受体轴已被确认为RAAS的负调节因子。ACE2将Ang II代谢为Ang(1-7),后者通过激活Mas受体具有与Ang II相反的特性。动物和人体研究均提供了强有力的证据表明,ACE2/Ang(1-7)/Mas受体轴对终末器官损伤具有保护作用。因此,ACE2/Ang(1-7)/Mas受体轴可能成为冠状动脉疾病和慢性肾衰竭的治疗靶点。

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Maladaptation of renal hemodynamics contributes to kidney dysfunction resulting from thoracic spinal cord injury in mice.肾脏血流动力学的失调导致了小鼠胸段脊髓损伤后的肾脏功能障碍。
Am J Physiol Renal Physiol. 2022 Aug 1;323(2):F120-F140. doi: 10.1152/ajprenal.00072.2022. Epub 2022 Jun 6.
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Insights into Cardiovascular Defects and Cardiac Epigenome in the Context of COVID-19.
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Effects of Angiotensin-(1-7) and Angiotensin II on Acetylcholine-Induced Vascular Relaxation in Spontaneously Hypertensive Rats.血管紧张素-(1-7)和血管紧张素 II 对自发性高血压大鼠乙酰胆碱诱导的血管舒张作用的影响。
Oxid Med Cell Longev. 2019 Nov 20;2019:6512485. doi: 10.1155/2019/6512485. eCollection 2019.
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