Abstract
Diabetic nephropathy (DN) is the main cause of end-stage renal disease. On the other hand, there are a couple of evidences, including human studies, which prove the role of epithelial mesenchymal transition (EMT) in pathophysiology of DN. EMT is characterized by loss of epithelial proteins and gain of mesenchymal markers. EMT is induced via three main conduit; TGFA�/Smad, integrin /ILK as well as Wnt/A�-catenin pathways. Besides, numerous studies illustrated how drugs and agents can modify this phenomenon. On the other hand, endothelial mesenchymal transition (EndoMT) has a well-known role in pathophysiology of diabetic nephropathy which has been studied in animal and human. Here, several drugs and modifiers which have been studied to ffigure out if they can amend nature of EMT or EndoMT are reported briefly. © 2018 The Author(s).
Highlights
Diabetic kidney disease (DKD) is a major complication of diabetes and is the single largest cause of endstage kidney failure [1]
The search was performed by using combinations of the following keywords and or their equivalents; epithelial mesenchymal transition, diabetic nephropathy, TGFβ/Smad, integrin /Integrin linked kinase (ILK), Wnt/β-catenin, diabetic kidney disease and endothelial mesenchymal transition
epithelial-mesenchymal transition (EMT) is induced via three main conduits, three main converging signaling pathways, which they are TGFβ/Smad, integrin/ILK, and Wnt/β-catenin pathways (Figure 1)
Summary
Diabetic kidney disease (DKD) is a major complication of diabetes and is the single largest cause of endstage kidney failure [1]. During the clinically silent stage, structural lesions include glomerular basement membrane thickening build up and extreme deposition of extracellular matrix (ECM) in the glomerulus and interstitial area. Leads to glomerulosclerosis and tubulointerstitial fibrosis as well [2,3]. Pathophysiology of diabetic nephropathy (DN) has intensively been studied. Two of them i.e. epithelial-mesenchymal transition (EMT) and endothelial-mesenchymal transition (EndoMT) are discussed here. A couple of drugs and agents which modify these phenomena are listed
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