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(Hypertension. 2008;52:816.)
© 2008 American Heart Association, Inc.

Editorial Commentaries

Angiotensin-Converting Enzyme 2

Cardioprotective Player in the Renin-Angiotensin System?

Anthony J. Turner

From the Institute of Molecular and Cellular Biology, University of Leeds, United Kingdom.

Correspondence to Prof Anthony J. Turner, Institute of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds LS2 9JT, UK. E-mail a.j.turner@leeds.ac.uk

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The first reports^1,2 of the angiotensin-converting enzyme (ACE) homolog, ACE2, in mid-2000 came almost 50 years after the discovery of ACE and, remarkably, its existence had not been predicted from the known physiology of the renin-angiotensin system (RAS) at the time. There has since been an exponential growth in knowledge of ACE2 functions,³ spanning such diverse areas of biology as cardiovascular function, liver disease, nutrition (eg, Hartnup disease), pregnancy, and, perhaps most unexpectedly, acute lung injury and severe acute respiratory syndrome (SARS), with ACE2 being the SARS virus receptor.⁴ It is now apparent that ACE2 contributes to the RAS through counterbalancing the action of ACE by converting angiotensin II to its metabolite angiotensin-(1-7) which, probably through the Mas receptor, brings about its vasodilatory and antiproliferative actions. Hence, ACE2 was quickly recognized as a possible cardioprotective activity and a potential target in controlling blood pressure.

Strategies to investigate the physiological and pathological roles of ACE2 have used either pharmacological approaches, for example by using inhibitors of ACE2 such as MLN4760, or transgenic approaches, neither of which have provided clearcut results. Indeed, studies with different strains of ACE2-null mice themselves have been ambiguous. In the first such study,⁵ ACE2 deletion resulted in increased plasma and tissue angiotensin II levels combined with associated cardiomyopathy and impaired cardiac contractility. These effects were reversed in mice in which both ACE and ACE2 were deleted, providing the first direct evidence that these 2 enzymes counterbalance each other in metabolism, presumably through regulating angiotensin II levels. However, . . . [Full Text of this Article]

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