Special Issue Article
Cellular and Molecular Basis of Epithelial-Mesenchymal Transition in Renal Fibrosis
Yoshiyuki Morishita* and Eiji Kusano
Division of Nephrology, Department of Medicine, Jichi Medical University, Tochigi, Japan
- *Corresponding Author:
- Y. Morishita
Division of Nephrology, Department of Medicine
Jichi Medical University, 3311-1, Yakushiji
Shimotsuke-city, Tochigi 329- 0498, Japan
E-mail: [email protected]
Received Date: August 24, 2011; Accepted Date: September 26, 2011; Published Date: October 19, 2011
Citation:Morishita Y, Kusano E (2011) Cellular and Molecular Basis of Epithelial- Mesenchymal Transition in Renal Fibrosis. J Nephrol Therapeutic S3:001. doi:10.4172/2161-0959.S3-001
Copyright: © Morishita Y, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Regardless of the underlying etiology, tubulointerstitial fibrosis is a common mechanism in the progression of chronic kidney disease (CKD) to end-stage renal disease. Epithelial-mesenchymal transition (EMT) of renal tubular cells plays an important role in tubulointerstitial fibrosis. Transforming growth factor-?1/Sma and Mad protein (TGF-?1/Smad) is thought to be a main signaling pathway for EMT of renal tubular cells. Progressive renal disease is also characterized histologically by an interstitial infiltrate of mononuclear cells. The chemokines secreted from renal tubular cells can trigger integrin-dependent adhesion of circulating mononuclear cells that leads to infiltration at tubulointerstitial space. The direct interaction of integrin lymphocyte function-associated antigen 1(LFA-1: ?L?2 integrin) on mononuclear cells and its ligand, intracellular adhesion molecule-1(ICAM-1) on renal tubular epithelial cells, contributes to a part of the EMT of renal tubular cells.