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
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.