Abstract
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.
Highlights
Regardless of the underlying etiology, tubulointerstitial fibrosis is a common mechanism in the progression of chronic kidney disease (CKD) to end-stage renal disease [1,2]
Several studies using a similar cell lineagetracing technique reported a substantial number of fibroblasts were derived from capillary endothelia which is a specialized type of epithelia by endothelial-to-mesenchymal transition [13,14]. These results strongly suggested that renal tubular epithelial cells and capillary endothelia migrated into interstitial space during Epithelial-mesenchymal transition (EMT)
Hertig et al [16] reported that de novo expression of vimentin of tubular epithelial cells in allograft kidney was significantly correlated with the progression of fibrosis
Summary
Regardless of the underlying etiology, tubulointerstitial fibrosis is a common mechanism in the progression of chronic kidney disease (CKD) to end-stage renal disease [1,2]. Epithelial-mesenchymal transition (EMT) of renal tubular cells, a process in which differentiated epithelial cells undergo transition to a fibroblast phenotype, plays an important role in renal fibrosis [3,4]. The cellular and molecular mechanism behind EMT has been increasingly understood as a result of basic and clinical studies in this field
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