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European Heart Journal Advance Access originally published online on January 25, 2005
European Heart Journal 2005 26(4):322-324; doi:10.1093/eurheartj/ehi043
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© The European Society of Cardiology 2005. All rights reserved. For Permissions, please e-mail: journals.permissions@oupjournals.org

ACE and ACE2: a tale of two enzymes

Lawrence S. Zisman*

Myomatrix Therapeutics, LLC

* One University Place, DB224 Rensselaer, NY 12144, USA. E-mail address: lzisman@myomatrix.com

This editorial refers to ‘Myocardial infarction increases ACE2 expression in rat and humans’{dagger} by Burrell et al., on page 369

The first 10% of the full text of this article appears below.

The cardiac renin–angiotensin–aldosterone system (RAAS) is an endocrine cascade, which results in the conversion of the inactive pro-hormone angiotensin I (Ang I) to the active peptide hormone Ang II, and may also function as an autocrine/paracrine system to modulate cardiac function and growth. Renin, the initial enzyme of this cascade, cleaves the amino terminus of the pre-pro-hormone angiotensinogen, thereby releasing the decapeptide pro-hormone Ang I. Angiotensin-converting enzyme (ACE) removes two additional amino acids to yield the active octapeptide hormone Ang II. Ang II, acting through the AT1 receptor, is a potent vasoconstrictor and stimulates cardiac growth. This cardiac growth may be related to myocyte hypertrophy and/or fibroblast proliferation with a concomitant alteration in the extracellular matrix. Ang II, by interaction with the . . . [Full Text of this Article]


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Related articles in EHJ:

Myocardial infarction increases ACE2 expression in rat and humans
Louise M. Burrell, John Risvanis, Eiji Kubota, Rachael G. Dean, Peter S. MacDonald, Sai Lu, Christos Tikellis, Sharon L. Grant, Rebecca A. Lew, A. Ian Smith, Mark E. Cooper, and Colin I. Johnston
EHJ 2005 26: 369-375. [Abstract] [Full Text]  



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