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First published online on January 25, 2008.
Experimental Physiology (2008)
DOI: 10.1113/expphysiol.2007.041350
© The Physiological Society 2008
A more recent version of this article appeared on May 1, 2008
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Received November 12, 2007
Revised December 19, 2007
Accepted after revision January 17, 2008

Renal [280]

ACE2 and the Kidney

Maria Jose Soler 1, Jan Wysocki 2, Daniel Batlle 2*

1 Universitat Autonoma de Barcelona.
2 Northwestern University

* To whom correspondence should be addressed. E-mail: d-batlle{at}northwestern.edu.


  Abstract
Angiotensin converting enzyme (ACE) 2 is a homologue of ACE with enzymatic activity that seems to counterbalance the angiotensin II promoting effect of ACE. Whereas ACE promotes angiotensin (Ang) II formation from Ang I, ACE2 degrades Ang II and Ang I. In this review, we cover recent studies that have delineated the localization of ACE2 within the kidney, an organ that highly expresses this enzyme. In models of diabetic kidney, pharmacological ACE2 inhibition is associated with albuminuria and worsening of glomerular injury. Similarly, genetic ablation of ACE2 causes glomerular lesions in male mice and worsens the renal lesions seen in the diabetic Akita mice. Altogether, these findings suggest that alterations in ACE2 may be involved in diabetic kidney disease, possibly by disrupting the metabolism of angiotensin peptides in such a way that angiotensin II degradation within the glomerulus may be diminished.

Key Words: Angiotensin, Enzyme, Renal




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Exp Physiol, May 1, 2008; 93(5): 517 - 518.
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