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Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors
Published on: June 7, 2016
Angiotensin-converting enzyme 2 and the kidney
Maria Jose Soler1, Jan Wysocki, Daniel Batlle
1Department of Nephrology, Hospital del Mar, Universitat Autònoma de Barcelona, Barcelona, Spain.
Experimental Physiology
|January 29, 2008
Summary
Reduced angiotensin-converting enzyme 2 (ACE2) activity in the kidneys may worsen diabetic kidney disease. This decline may disrupt angiotensin peptide metabolism, diminishing angiotensin II degradation and increasing glomerular injury.
Area of Science:
- Nephrology
- Endocrinology
- Cardiovascular Research
Background:
- Angiotensin-converting enzyme (ACE) 2 counterbalances ACE's effects on angiotensin II.
- ACE2 degrades both Angiotensin II and Angiotensin I.
- The kidney highly expresses ACE2, suggesting a crucial renal role.
Purpose of the Study:
- To review recent studies on ACE2 localization in the kidney.
- To explore the role of ACE2 in diabetic kidney disease.
- To understand how ACE2 dysfunction impacts renal pathology.
Main Methods:
- Review of recent scientific literature.
- Analysis of studies involving pharmacological ACE2 inhibition in diabetic kidney models.
- Examination of genetic ablation studies of ACE2 in mice, including diabetic models.
Main Results:
- Pharmacological ACE2 inhibition in diabetic kidney models correlates with albuminuria and worsened glomerular injury.
- Genetic ACE2 ablation causes glomerular lesions in male mice.
- ACE2 deficiency exacerbates renal lesions in diabetic Akita mice.
Conclusions:
- Decreased ACE2 may contribute to diabetic kidney disease pathogenesis.
- Disrupted angiotensin peptide metabolism, specifically reduced Angiotensin II degradation, is a potential mechanism.
- ACE2 is a potential therapeutic target for diabetic kidney disease.
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