Open AccessACE and ACE2 in kidney disease
Author(s) -
Sonoo Mizuiri
Publication year - 2015
Publication title -
world journal of nephrology
Language(s) - English
Resource type - Journals
ISSN - 2220-6124
DOI - 10.5527/wjn.v4.i1.74
Subject(s) - angiotensin ii , renin–angiotensin system , endocrinology , angiotensin converting enzyme 2 , angiotensin ii receptor type 1 , medicine , catabolism , kidney , vasoconstriction , disease , receptor , metabolism , blood pressure , covid-19 , infectious disease (medical specialty)
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.