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• W2013990588 abstract "Pulmonary arterial hypertension (PAH) is a progressive disease with poor survival outcome. The presence of PAH increases morbidity and reduces survival in patients with congenital heart disease (CHD) [ [1] Simonneau G. Gatzoulis M.A. Adatia I. et al. Updated clinical classification of pulmonary hypertension. J Am Coll Cardiol. 2013; 62: D34-D41 Crossref PubMed Scopus (2075) Google Scholar ]. The field of CHD–PAH has seen dramatic progress over the last two decades with improved survival and quality of life for patients, however, this remains a deadly and debilitating disease [ [2] D'Alto M. Diller G.P. Pulmonary hypertension in adults with congenital heart disease and Eisenmenger syndrome: current advanced management strategies. Heart. 2014; 100: 1322-1328 Crossref PubMed Scopus (43) Google Scholar ]. The exact pathogenesis of CHD–PAH is poorly understood, therapeutic options for those patients are limited. The angiotensin (Ang) converting enzyme 2 (ACE2)-Ang-(1–7)-Mas receptor axis is an important component of the renin-angiotensin system, ACE2 coverts Ang II into Ang-(1–7), which exerts both vasodilatory and anti-proliferative effects [ 3 Ferreira A.J. Shenoy V. Yamazato Y. et al. Evidence for angiotensin-converting enzyme 2 as a therapeutic target for the prevention of pulmonary hypertension. Am J Respir Crit Care Med. 2009; 179: 1048-1054 Crossref PubMed Scopus (221) Google Scholar , 4 Shenoy V. Qi Y. Katovich M.J. Raizada M.K. ACE2, a promising therapeutic target for pulmonary hypertension. Curr Opin Pharmacol. 2011; 11: 150-155 Crossref PubMed Scopus (91) Google Scholar ]. Recent studies have demonstrated the therapeutic effects of Ang-(1–7) in monocrotaline-induced PAH model [ 5 Shenoy V. Ferreira A.J. Qi Y. et al. The ACE2/Ang-(1–7)/MAS axis confers cardiopulmonary protection against lung fibrosis and pulmonary hypertension. Am J Respir Crit Care Med. 2010; 182: 1065-1072 Crossref PubMed Scopus (211) Google Scholar , 6 Chen L. Xiao J. Li Y. Ma H. Ang-(1–7) might prevent the development of monocrotaline induced pulmonary arterial hypertension in rats. Eur Rev Med Pharmacol Sci. 2011; 15: 1-7 PubMed Google Scholar ]. Our previous study showed that serum ACE2 levels and activity were decreased in the patients with CHD–PAH [ 7 Dai H.L. Guo Y. Guang X.F. Xiao Z.C. Zhang M. Yin X.L. The changes of serum angiotensin-converting enzyme 2 in patients with pulmonary arterial hypertension due to congenital heart disease. Cardiology. 2013; 124: 208-212 Crossref PubMed Scopus (29) Google Scholar , 8 Dai H.L. Guo Y. Yin X.L. Guang X.F. Lu Y.B. Zhang W.H. The changes of serum angiotensin-converting enzyme 2 activity in patients with pulmonary arterial hypertension due to congenital heart disease (in Chinese). Chin J Cardiovasc Res. 2013; 11: 481-483 Google Scholar ]. In this study, we explored the hypothesis that serum Ang-(1–7) levels was also decreased in the patients with CHD–PAH." @default.
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• W2013990588 date "2014-10-01" @default.
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• W2013990588 title "Decreased levels of serum Angiotensin-(1–7) in patients with pulmonary arterial hypertension due to congenital heart disease" @default.
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• W2013990588 doi "https://doi.org/10.1016/j.ijcard.2014.08.021" @default.
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