Key result
A decrease in ACE2 may be involved in diabetic kidney disease by disrupting the metabolism of angiotensin peptides and diminishing angiotensin II degradation within the glomerulus.
Why the study?
Does ACE2 inhibition or ablation worsen glomerular injury in models of diabetic kidney disease?
Does ACE2 inhibition or ablation worsen glomerular injury in models of diabetic kidney disease?
A decrease in ACE2 may be involved in the pathogenesis of diabetic kidney disease by diminishing angiotensin II degradation within the glomerulus.
ACE2 inhibition may worsen albuminuria in diabetic kidney models; leaves open therapeutic targeting in patients.
Angiotensin-converting enzyme (ACE) 2 is a homologue of ACE with enzymatic activity that seems to counterbalance the angiotensin II-promoting effect of ACE. While ACE promotes angiotensin (Ang) II formation from Ang I, ACE2 degrades Ang II and Ang I. In this review, we discuss 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 diabetic Akita mice. Taken together, these findings suggest that a decrease 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.
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Soler et al. (2008) conducted a review in Diabetic kidney disease. ACE2 inhibition or genetic ablation was evaluated. A decrease in ACE2 may be involved in diabetic kidney disease by disrupting the metabolism of angiotensin peptides and diminishing angiotensin II degradation within the glomerulus.
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