Abstract
Pulmonary arterial hypertension (PAH) is an incurable fatal disease, with the mechanism of imbalance of vascular contraction and relaxation which start as a series of pathophysiological reactions. Angiotensin-converting enzyme 2-angiotensin (1-7)-G protein-coupled receptor axis [ACE2-Ang(1-7)-Mas], an expanded vascular axis which is considered as new axis of renin-angiotensin system (RAS) is a negative regulator of the classical angiotensin-converting enzyme-angiotensin Ⅱ-angiotensin Ⅱ type 1 receptor axis (ACE-AngⅡ-AT1R), a contraction vessel, proliferation axis. A retrospective study concerning the pathophysiological mechanism of ACE2 in the treatment of PAH was done and found that ACE2-Ang-(1-7)-Mas axis could reduce PAH induced by monocrotaline (MCT) through declining the inflammatory cascade, improving endothelial dysfunction and regulating autonomic nerve, reduce PAH induced by hypoxia through inhibiting the proliferation of pulmonary artery smooth muscle cells and reduce PAH induced by congenital heart disease. Therefore, ACE2 may become a future drug of preventing and treating PAH. Key words: Angiotensin-converting enzyme 2; Pulmonary arterial hypertension; Renin angiotensin system; Angiotensin
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