Current Heart Failure Reports

, Volume 8, Issue 3, pp 176–183

Recombinant Human Angiotensin-Converting Enzyme 2 as a New Renin-Angiotensin System Peptidase for Heart Failure Therapy

Article

DOI: 10.1007/s11897-011-0063-7

Cite this article as:
Oudit, G.Y. & Penninger, J.M. Curr Heart Fail Rep (2011) 8: 176. doi:10.1007/s11897-011-0063-7

Abstract

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.

Keywords

Angiotensin converting enzyme 2ACE2Angiotensin 1-7Ang 1-7Angiotensin IIAng IINADPH oxidaseDiastolic dysfunctionChymaseSignalingMyocardial fibrosisHypertrophyHeart failureTherapyRecombinant human angiotensin converting enzyme 2RhACE2Diastolic dysfunction

Copyright information

© Springer Science+Business Media, LLC 2011

Authors and Affiliations

  1. 1.Department of Physiology, Division of Cardiology, Department of Medicine, Mazankowski Alberta Heart InstituteUniversity of AlbertaEdmontonCanada
  2. 2.Institute of Molecular BiotechnologyViennaAustria