scholarly journals Angiotensin-Converting Enzyme 2 as a Therapeutic Target for Heart Failure

2013 ◽  
Vol 11 (1) ◽  
pp. 58-63 ◽  
Author(s):  
Mohammed A. R. Chamsi-Pasha ◽  
Zhili Shao ◽  
W. H. Wilson Tang
2014 ◽  
Vol 92 (7) ◽  
pp. 558-565 ◽  
Author(s):  
Nirmal Parajuli ◽  
Tharmarajan Ramprasath ◽  
Vaibhav B. Patel ◽  
Wang Wang ◽  
Brendan Putko ◽  
...  

Angiotensin-converting enzyme 2 (ACE2) is a monocarboxypeptidase that metabolizes several vasoactive peptides, including angiotensin II (Ang-II; a vasoconstrictive/proliferative peptide), which it converts to Ang-(1–7). Ang-(1–7) acts through the Mas receptor to mediate vasodilatory/antiproliferative actions. The renin–angiotensin system involving the ACE–Ang-II–Ang-II type-1 receptor (AT1R) axis is antagonized by the ACE2–Ang-(1–7)–Mas receptor axis. Loss of ACE2 enhances adverse remodeling and susceptibility to pressure and volume overload. Human recombinant ACE2 may act to suppress myocardial hypertrophy, fibrosis, inflammation, and diastolic dysfunction in heart failure patients. The ACE2–Ang-(1–7)–Mas axis may present a new therapeutic target for the treatment of heart failure patients. This review is mainly focused on the analysis of ACE2, including its influence and potentially positive effects, as well as the potential use of human recombinant ACE2 as a novel therapy for the treatment cardiovascular diseases, such as hypertension and heart failure.


Author(s):  
Iman Razeghian-Jahromi ◽  
Mohammad Javad Zibaeenezhad ◽  
Zhibing Lu ◽  
Elyaspour Zahra ◽  
Razmkhah Mahboobeh ◽  
...  

2008 ◽  
Vol 52 (9) ◽  
pp. 750-754 ◽  
Author(s):  
Slava Epelman ◽  
W.H. Wilson Tang ◽  
Stephen Y. Chen ◽  
Frederick Van Lente ◽  
Gary S. Francis ◽  
...  

2020 ◽  
Vol 41 (19) ◽  
pp. 1810-1817 ◽  
Author(s):  
Iziah E Sama ◽  
Alice Ravera ◽  
Bernadet T Santema ◽  
Harry van Goor ◽  
Jozine M ter Maaten ◽  
...  

Abstract Aims The current pandemic coronavirus SARS-CoV-2 infects a wide age group but predominantly elderly individuals, especially men and those with cardiovascular disease. Recent reports suggest an association with use of renin–angiotensin–aldosterone system (RAAS) inhibitors. Angiotensin-converting enzyme 2 (ACE2) is a functional receptor for coronaviruses. Higher ACE2 concentrations might lead to increased vulnerability to SARS-CoV-2 in patients on RAAS inhibitors. Methods and results We measured ACE2 concentrations in 1485 men and 537 women with heart failure (index cohort). Results were validated in 1123 men and 575 women (validation cohort). The median age was 69 years for men and 75 years for women. The strongest predictor of elevated concentrations of ACE2 in both cohorts was male sex (estimate = 0.26, P < 0.001; and 0.19, P < 0.001, respectively). In the index cohort, use of ACE inhibitors, angiotensin receptor blockers (ARBs), or mineralocorticoid receptor antagonists (MRAs) was not an independent predictor of plasma ACE2. In the validation cohort, ACE inhibitor (estimate = –0.17, P = 0.002) and ARB use (estimate = –0.15, P = 0.03) were independent predictors of lower plasma ACE2, while use of an MRA (estimate = 0.11, P = 0.04) was an independent predictor of higher plasma ACE2 concentrations. Conclusion In two independent cohorts of patients with heart failure, plasma concentrations of ACE2 were higher in men than in women, but use of neither an ACE inhibitor nor an ARB was associated with higher plasma ACE2 concentrations. These data might explain the higher incidence and fatality rate of COVID-19 in men, but do not support previous reports suggesting that ACE inhibitors or ARBs increase the vulnerability for COVID-19 through increased plasma ACE2 concentrations.


2014 ◽  
Vol 127 (4) ◽  
pp. 243-249 ◽  
Author(s):  
Daniel W. Lambert ◽  
Louise A. Lambert ◽  
Nicola E. Clarke ◽  
Nigel M. Hooper ◽  
Karen E. Porter ◽  
...  

The molecular mechanisms controlling the expression of ACE2, a critical regulator of cardiovascular homoeostasis, remain poorly defined. In the present study, we show that miR-421 regulates expression of ACE2 in cardiac myofibroblasts, identifying a possible new therapeutic target in cardiovascular disease.


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