Abstract
Endothelial dysfunction and tubulointerstitial fibrosis are characteristics of diabetic kidneys. Recent evidence has suggested that the diabetic kidney is associated with dipeptidyl peptidase (DPP)-4 overexpression in endothelial cells. Several insults can induce endothelial cells to alter their phenotype into a mesenchymal-like phenotype via endothelial-mesenchymal transition (EndMT), which plays pivotal roles in tissue fibrosis. We have recently revealed the fibrogenic role of DPP-4 through the induction of EndMT in diabetic kidneys. This review mainly focuses on the biological and pathological significance of DPP-4 overexpression in endothelial cells through the mechanisms of endothelial homeostasis defects, EndMT, and kidney fibrosis.
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