Journal
NEPHROLOGIE & THERAPEUTIQUE
Volume 4, Issue -, Pages S25-S28Publisher
ELSEVIER MASSON
DOI: 10.1016/S1769-7255(08)73648-4
Keywords
chronic allograft nephropathy; interstitial fibrosis; epithelial-mesenchymal transition; tubular atrophy
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About 40% of renal graft losses over 10 years in Europe are caused by fibrosis. To explain the origin of interstitial. fibroblasts, the epithelial-mesenchymal. transition (EMT) theory has been recently ventured : under the effect of an aggression, tubutar epithelial cells may change into fibroblasts, cross over the basal membrane, and join interstitium. This innovative hypothesis has been confirmed by the finding of a fibrobtast-specific protein FSP-1 in the tubular epithelium, then by the detection of fibroblast-like FSP-1 expressing cells in the proximal tubule by confocal. microscopy in a transgenic murine model in which fibrosis has been induced. In the renal graft, EMT markers such as FSP-1 and vimentin, have been detected in tubular epithelium in case of chronic allograft nephropathy, correlatively to the loss of expression of epithelial markers. The expression of EMT markers takes place very early, in the first months post-transplantation, in transplant patients whose renal function is not yet impaired, suggesting the existence of a patho-physiotogical link between EMT markers expression and graft fibrosis development. (C) 2008 Elsevier Masson SAS et Association Societe de Nephrologie. Tous droits reserves.
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