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Submitted: 03 Jul 2017
Accepted: 10 Sep 2017
ePublished: 04 Dec 2017
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J Renal Inj Prev. 2018;7(1): 1-6.
doi: 10.15171/jrip.2018.01

Scopus ID: 85042607933
  Abstract View: 4319
  PDF Download: 2127

Mini-Review

Epithelial and endothelial mesenchymal transition and their role in diabetic kidney disease

Farahnaz Dadras 1, Vida Sheikh 2, Farhad Khoshjou 2*

1 Department of Internal Medicine, Section of Nephrology, Iran University of Medical Sciences, Tehran, Iran
2 Clinical Research Development unit of Shahid Beheshti Hospital, Hamadan University of Medical Sciences, Hamadan, Iran
*Corresponding Author: *Corresponding author: Farhad Khoshjou,, Email: fakhoshjou@yahoo.com

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; TGFβ/Smad, integrin /ILK as well as Wnt/β-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

 Implication for health policy/practice/research/medical education:

Diabetes and its complications including diabetic nephropathy are spreading worldwide. On the other hand, pathophysiology of diabetic kidney disease and its modifiers have been studied broadly. This mini-review presents a couple of them, allocated to EMT and Endomt, briefly and to the point.

Please cite this paper as: Dadras F, Sheikh V, Khoshjou F. Epithelial and endothelial mesenchymal transition and their role in diabetic kidney disease. J Renal Inj Prev. 2018;7(1):1-6. DOI: 10.15171/jrip.2018.01.

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