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Recombinant Human Angiotensin-Converting Enzyme 2 as a New Renin-Angiotensin System Peptidase for Heart Failure Therapy.
MedLine Citation:
PMID:  21611889     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
Angiotensin-converting enzyme 2 (ACE2) is a monocarboxypeptidase that metabolizes several peptides, including the degradation of angiotensin (Ang) II, a peptide with vasoconstrictive/proliferative effects, to generate Ang 1-7, which exerts vasodilatory/antiproliferative actions by acting through its receptor Mas. ACE2 is a multifunctional enzyme, and its actions on other vasoactive peptides, including the apelin-13 and apelin-17 peptides, also can contribute to its cardiovascular effects. The classical pathway of the renin-angiotensin system involving the ACE-Ang II-Ang II type-1 receptor axis is antagonized by the second arm constituted by the ACE2/Ang 1-7/Mas receptor axis. Loss of ACE2 enhances the adverse pathological remodeling susceptibility to pressure overload and myocardial infarction. Human recombinant ACE2 also is a negative regulator of Ang II-induced myocardial hypertrophy, fibrosis, and diastolic dysfunction and suppresses pressure overload-induced heart failure. Due to its characteristics, the ACE2/Ang 1-7/Mas axis may represent new possibilities for developing novel therapeutic strategies for the treatment of hypertension and heart failure. This review summarizes the beneficial effects of ACE2 in heart disease and the potential use of human recombinant ACE2 as a novel therapy for heart failure.
Authors:
Gavin Y Oudit; Josef M Penninger
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2011-5-26
Journal Detail:
Title:  Current heart failure reports     Volume:  -     ISSN:  1546-9549     ISO Abbreviation:  -     Publication Date:  2011 May 
Date Detail:
Created Date:  2011-5-25     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101196487     Medline TA:  Curr Heart Fail Rep     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Affiliation:
Department of Physiology, Division of Cardiology, Department of Medicine, Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, Alberta, T6G 2S2, Canada, gavin.oudit@ualberta.ca.
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