Onset of Experimental Severe Cardiac Fibrosis Is Mediated by Overexpression of Angiotensin-Converting Enzyme 2
Rachel Masson, Stuart A Nicklin, Margaret Anne Craig, Martin McBride, Kirsten Gilday, Paul Gregorevic, James M Allen, Jeffrey S Chamberlain, Godfrey Smith, Delyth Graham, Anna F Dominiczak, Claudio Napoli, Andrew H Baker
HYPERTENSION | LIPPINCOTT WILLIAMS & WILKINS | Published : 2009
Angiotensin-converting enzyme (ACE) 2 is a recently identified homologue of ACE. There is great interest in the therapeutic benefit for ACE2 overexpression in the heart. However, the role of ACE2 in the regulation of cardiac structure and function, as well as maintenance of systemic blood pressure, remains poorly understood. In cell culture, ACE2 overexpression led to markedly increased myocyte volume, assessed in primary rabbit myocytes. To assess ACE2 function in vivo, we used a recombinant adeno-associated virus 6 delivery system to provide 11-week overexpression of ACE2 in the myocardium of stroke-prone spontaneously hypertensive rats. ACE2, as well as the ACE inhibitor enalapril, signif..View full abstract
Awarded by British Heart Foundation
Awarded by NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES
This work was supported by the British Heart Foundation (PG/07/015/22372).