2010
DOI: 10.1016/j.ijcard.2009.11.057
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Angiotensin converting enzyme 2 gene expression increased compensatory for left ventricular remodeling in patients with end-stage heart failure

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Cited by 42 publications
(36 citation statements)
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“…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.…”
Section: Angiotensin-converting Enzyme 2 As a Component Of The Ansupporting
confidence: 69%
See 1 more Smart Citation
“…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.…”
Section: Angiotensin-converting Enzyme 2 As a Component Of The Ansupporting
confidence: 69%
“…ACE2 is widely distributed in many tissues with higher levels in the heart, kidney, and testis (Batlle et al, 2006, 2008; Ferrario & Varagic, 2010; Ferrario et al, 2005a, 2005b; Gembardt et al, 2005; Hamming et al, 2004, 2008; Ohtsuki et al, 2010; Oudit et al, 2006). Our studies showed that ACE2-dependent Ang-(1–7) formation from Ang II was significantly higher from the heart of hypertensive rats as compared to normal rat heart (Trask et al, 2007).…”
Section: Angiotensin-converting Enzyme 2 As a Component Of The Anmentioning
confidence: 99%
“…On the other side, increased ACE2 mRNA, protein, and activity were reported in failing human hearts (2427) and several experimental models of myocardial infarction (16;25). Moreover, ACE2 activity in plasma of heart failure patients increased as well and correlates with unfavorable clinical outcomes (6;28).…”
Section: Ace2 and Cardiac Diseasementioning
confidence: 99%
“…Interestingly, there was a strong relationship between the amount of ACE2 gene expression and the severity of LV remodeling determined by LV dimensions [31], suggesting that ACE2 expression could be activated as an adaptive compensatory mechanism to militate against LV remodeling. However, ACE2 expression did not correlate with either LV ejection fraction nor plasma BNP levels, implying that such compensatory increased expression of ACE2 may be insufficient to counter pathologic processes as disease progressed [31]. …”
Section: Role Of Ace2 In Cardiac Remodeling and Systolic Dysfunction mentioning
confidence: 99%