The pathological significance of dipeptidyl peptidase-4 in endothelial cell homeostasis and kidney fibrosis

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.