Angiotensin converting enzyme 2 and the kidney

被引:21
|
作者
Ortiz-Melo, David I.
Gurley, Susan B. [1 ]
机构
[1] Duke Univ, Div Nephrol, Dept Med, Durham, NC 27710 USA
来源
关键词
angiotensin converting enzyme 2; angiotensin II; kidney; renin-angiotensin system; OXIDATIVE STRESS; BLOOD-PRESSURE; DIABETIC-NEPHROPATHY; GLOMERULAR INJURY; URINARY ACE2; EXPRESSION; RECEPTOR; OVEREXPRESSION; RENIN; MICE;
D O I
10.1097/MNH.0000000000000182
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Purpose of reviewAngiotensin-converting enzyme 2 (ACE2) is a monocarboxypeptidase that metabolizes angiotensin II (AngII). AngII levels can be modulated by ACE2 in tissues where the enzyme is highly expressed, such as the kidney. In the kidney, ACE2 has the potential to regulate the intrarenal renin-angiotensin system (RAS), which can impact blood pressure and renal injury. Thus, in disease states where the RAS is often upregulated, the function of ACE2 plays a particularly important role. This review highlights the results of recent studies that demonstrate the interplay between ACE2 and the kidney under normal and pathological conditions.Recent findingsACE2 has been reported to play a key role in renal and cardiovascular function. Recent studies have implicated shedding of the membrane-bound ectodomain of ACE2 as one way in which the enzyme can be regulated and enzymatic activity altered. This posttranslational modification releases a fragment which retains enzymatic activity, and thus provides a novel mechanism by which the RAS can be altered in response to physiological stimuli. Decreased ACE2 activity is associated with increased blood pressure, diabetes, and oxidative stress, whereas, increased levels of ACE2 appear to be renoprotective.SummaryA growing body of evidence, involving both experimental and human studies, points out the crucial role that ACE2 plays on the modulation of renal injury. Thus, therapeutic targets aiming to increase ACE2 activity and the ACE2-Ang(1-7)-MasR axis could potentially become clinically relevant, especially in disease states where the renal RAS is upregulated.
引用
收藏
页码:59 / 66
页数:8
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