Key result
This review discusses alterations in circulating and renal ACE2 across different renal pathologies, highlighting a dissociation between tubular and glomerular ACE2 expression in diabetic kidney disease.
This review highlights the differential alterations of ACE2 expression in tubular versus glomerular compartments in various kidney diseases.
Compartment-specific ACE2 patterns in diabetic kidney disease merit targeted investigation; leaves open any therapeutic implications for renin-angiotensin modulation.
Angiotensin-converting enzyme 2 (ACE2) is a monocarboxypeptidase that degrades angiotensin (Ang) II to Ang-(1-7). ACE2 is highly expressed within the kidneys, it is largely localized in tubular epithelial cells and less prominently in glomerular epithelial cells and in the renal vasculature. ACE2 activity has been shown to be altered in diabetic kidney disease, hypertensive renal disease and in different models of kidney injury. There is often a dissociation between tubular and glomerular ACE2 expression, particularly in diabetic kidney disease where ACE2 expression is increased at the tubular level but decreased at the glomerular level. In this review, we will discuss alterations in circulating and renal ACE2 recently described in different renal pathologies and disease models as well as their possible significance.
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Soler et al. (2013) conducted a review in Kidney disease. ACE2 alterations was evaluated. This review discusses alterations in circulating and renal ACE2 across different renal pathologies, highlighting a dissociation between tubular and glomerular ACE2 expression in diabetic kidney disease.
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