Abstract
In renal grafts, the progression of interstitial fibrosis and tubular atrophy (IF/TA) is exponential during the first months post-transplant. Consequently, roughly 40% of the cadaveric grafts will function less than ten years. There is, however, no specific strategy to halt fibrogenesis, i.e. the progression of fibrosis with time, in kidney recipients. Epithelial to mesenchymal transition (EMT) is a biological process used to disperse cells during embryogenesis. In the setting of injury, it is also a mechanism to escape cellular death. The last five years, several studies demonstrated that EMT does occur in tubular epithelial cells, which have been shown to loose the expression of epithelial markers, and acquire the expression of mesenchymal proteins, like vimentin. The aim of this review is triple: 1) discuss the connections between EMT and the context of transplantation; 2) explain how EMT markers may be useful in clinical practice, as promising surrogate markers for fibrogenesis; 3) discuss some therapeutic perspectives.
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