%0 Journal Article
%T Epithelial to mesenchymal transition as a biomarker in renal fibrosis: are we ready for the bedside?
%A Pierre Galichon
%A Alexandre Hertig
%J Fibrogenesis & Tissue Repair
%D 2011
%I BioMed Central
%R 10.1186/1755-1536-4-11
%X 'What is simple is false, and what is complex is unusable'Paul Val¨Śry (1941)Since its first description by Elisabeth Hay, epithelial to mesenchymal transition (EMT) has raised increasing interest. One reason for this is that the concept has extended from embryology to pathology. It was first defined in embryological studies as a process that is instrumental to organogenesis, in which cells lose their epithelial phenotype, acquire mesenchymal features, and migrate to generate new organs in the embryo [1]. This phenomenon, now called Type 1 EMT [2], is replicated in Type 3 EMT, conferring on cancerous cells the ability to disseminate by metastasis and to resist chemotherapy [3]. Type 2 EMT refers to the rather startling concept that epithelial cells subjected to injury may undergo similar transformations and thus provide new fibroblasts in the interstitium.EMT was first associated with fibrogenesis 15 years ago, with the observation of renal tubular epithelial cells aberrantly expressing fibroblast-specific protein (FSP)1 in a model of mouse anti-tubular membrane disease[4]. This led Strutz et al. to hypothesize that some fibroblasts might be derived from transformed epithelial cells. This hypothesis was confirmed when Iwano showed that tubular epithelial cells bearing the reporter gene lacZ massively contributed to the pool of interstitial fibroblasts (up to 36% of all fibroblasts) in a model of mouse renal fibrosis induced by unilateral ureteral obstruction [5]. The study of renal EMT raised even more interest and hopes in the nephrological community 1 year later, when Zeisberg et al. showed that bone morphogenetic protein (BMP)7 could reverse EMT in mice exposed to nephrotoxic serum and even reverse renal fibrosis itself [6].However, several studies have subsequently contested the reality of EMT in renal fibrosis. Fate-tracing experiments on tubular epithelial cells in various animal models (Habu venom plus angiotensin 2 in rats, unilateral ureteral obstruction or
%U http://www.fibrogenesis.com/content/4/1/11