Angiotensin-converting enzyme 2 is an essential regulator of heart function

Michael A. Crackower, Renu Sarao, Gavin Y. Oudit, Chana Yagil, Ivona Kozieradzki, Sam E. Scanga, Antonio J. Oliveira-dos-Santos, Joan da Costa, Liyong Zhang, York Pei, James Scholey, Carlos M. Ferrario, Armen S. Manoukian, Mark C. Chappell, Peter H. Backx, Yoram Yagil and Josef M. Penninger ()
Additional contact information
Michael A. Crackower: Amgen Research Institute/Ontario Cancer Institute, University of Toronto
Renu Sarao: Amgen Research Institute/Ontario Cancer Institute, University of Toronto
Gavin Y. Oudit: The Heart & Stroke/Richard Lewar Centre for Excellence in Cardiovascular Research, University of Toronto
Chana Yagil: Faculty of Health Science, Ben-Gurion University Barzilai Medical Center Campus
Ivona Kozieradzki: Amgen Research Institute/Ontario Cancer Institute, University of Toronto
Sam E. Scanga: University Health Network, Ontario Cancer Institute, University of Toronto
Antonio J. Oliveira-dos-Santos: Amgen Research Institute/Ontario Cancer Institute, University of Toronto
Joan da Costa: Amgen Research Institute/Ontario Cancer Institute, University of Toronto
Liyong Zhang: Amgen Research Institute/Ontario Cancer Institute, University of Toronto
York Pei: University of Toronto
James Scholey: University of Toronto
Carlos M. Ferrario: The Hypertension and Vascular Disease Center, Wake Forest University School of Medicine
Armen S. Manoukian: University Health Network, Ontario Cancer Institute, University of Toronto
Mark C. Chappell: The Hypertension and Vascular Disease Center, Wake Forest University School of Medicine
Peter H. Backx: The Heart & Stroke/Richard Lewar Centre for Excellence in Cardiovascular Research, University of Toronto
Yoram Yagil: University of Toronto
Josef M. Penninger: Amgen Research Institute/Ontario Cancer Institute, University of Toronto

Nature, 2002, vol. 417, issue 6891, 822-828

Abstract: Abstract Cardiovascular diseases are predicted to be the most common cause of death worldwide by 2020. Here we show that angiotensin-converting enzyme 2 (ace2) maps to a defined quantitative trait locus (QTL) on the X chromosome in three different rat models of hypertension. In all hypertensive rat strains, ACE2 messenger RNA and protein expression were markedly reduced, suggesting that ace2 is a candidate gene for this QTL. Targeted disruption of ACE2 in mice results in a severe cardiac contractility defect, increased angiotensin II levels, and upregulation of hypoxia-induced genes in the heart. Genetic ablation of ACE on an ACE2 mutant background completely rescues the cardiac phenotype. But disruption of ACER, a Drosophila ACE2 homologue, results in a severe defect of heart morphogenesis. These genetic data for ACE2 show that it is an essential regulator of heart function in vivo.

Date: 2002
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DOI: 10.1038/nature00786

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