“…Earlier, a study from Huentelman et al (2005) found that ACE2 overexpression induced by intracardiac injection of a lentiviral vector encoding the mouse ACE2 attenuated the development of Ang II-induced cardiac hypertrophy and fibrosis. Additional studies agree with the conclusion that ACE2 counteracts cardiac remodeling induced by myocardial injury, renal hypertension, and heart failure, as well as retarding the progression of atherosclerosis and vascular injury (Burgelova et al, 2009; Burrell et al, 2005; Crackower et al, 2002; Diez-Freire et al, 2006; Dong et al, 2008; Epelman et al, 2008; Ferrario, 2005; Ferrario et al, 2005a; Goulter et al, 2004; Grobe et al, 2007a, 2007b; Hamming et al, 2008; Heeneman et al, 2007; Hu et al, 2007; Igase et al, 2005, 2008; Ji et al, 2008; Kaiqiang et al, 2009; Kassiri et al, 2009; Lovren et al, 2008; Ohtsuki et al, 2010; Pan et al, 2007; Sluimer et al, 2008; Trask et al, 2010; Varagic et al, 2010; Velkoska et al, 2010; Yamamoto et al, 2006; Zulli et al, 2006). These findings demonstrate that ACE2 plays a central role in balancing the pressor and proliferative activity of the ACE/Ang II/AT 1 receptor axis.…”