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Copyright ©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Nephrol. Feb 6, 2015; 4(1): 74-82
Published online Feb 6, 2015. doi: 10.5527/wjn.v4.i1.74
ACE and ACE2 in kidney disease
Sonoo Mizuiri, Yasushi Ohashi
Sonoo Mizuiri, Department of Nephrology, Ichiyokai Harada Hospital, Hiroshima-Shi 731-5134, Japan
Sonoo Mizuiri, Yasushi Ohashi, Department of Nephrology, Toho University School of Medicine, Tokyo 143-8540, Japan
Author contributions: Both authors contributed to this work.
Supported by The Toho University School of Medicine Research Foundation.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Sonoo Mizuiri, MD, PhD, Department of Nephrology, Ichiyokai Harada Hospital, 7-10 Kairoyama-Cho, Saeki-Ku, Hiroshima-Shi 731-5134, Japan. sm210@med.toho-u.ac.jp
Telephone: +81-82-9235161 Fax: +81-82-9218035
Received: June 25, 2014
Peer-review started: June 26, 2014
First decision: July 10, 2014
Revised: July 16, 2014
Accepted: October 27, 2014
Article in press: October 27, 2014
Published online: February 6, 2015
Processing time: 226 Days and 16.3 Hours
Abstract

Renin angiotensin system (RAS) activation has a significant influence on renal disease progression. The classical angiotensin-converting enzyme (ACE)-angiotensin II (Ang II)-Ang II type 1 (AT1) axis is considered to control the effects of RAS activation on renal disease. However, since its discovery in 2000 ACE2 has also been demonstrated to have a significant impact on the RAS. The synthesis and catabolism of Ang II are regulated via a complex series of interactions, which involve ACE and ACE2. In the kidneys, ACE2 is expressed in the proximal tubules and less strongly in the glomeruli. The synthesis of inactive Ang 1-9 from Ang I and the catabolism of Ang II to produce Ang 1-7 are the main functions of ACE2. Ang 1-7 reduces vasoconstriction, water retention, salt intake, cell proliferation, and reactive oxygen stress, and also has a renoprotective effect. Thus, in the non-classical RAS the ACE2-Ang 1-7-Mas axis counteracts the ACE-Ang II-AT1 axis. This review examines recent human and animal studies about renal ACE and ACE2.

Keywords: Angiotensin-converting enzyme; Angiotensin-converting enzyme 2; Diabetic nephropathy; Kidney disease; Renin angiotensin system

Core tip: In the kidneys, angiotensin-converting enzyme 2 (ACE2) is expressed in the proximal tubules and less strongly in the glomeruli. The synthesis of inactive Ang 1-9 from angiotensin I (Ang I) and the catabolism of Ang II to produce Ang 1-7 represent the main functions of ACE2. Ang 1-7 reduces vasoconstriction, water retention, salt intake, cell proliferation, and reactive oxygen stress, and also has a renoprotective effect. Thus, in the non-classical renin angiotensin system the ACE2-Ang 1-7-Mas axis counteracts the ACE-Ang II-AT1 axis. This review examines recent human and animal studies about ACE and ACE2 expression in various renal diseases.