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EMT-MET in renal disease: should we curb our enthusiasm?
Pierre Galichon1, Serge Finianos, Alexandre Hertig
1Institut National de la Santé et de la Recherche Médicale (INSERM) Unité Mixte de Recherche (UMR) S 702, France; APHP, Hôpital Tenon, Urgences Néphrologiques et Transplantation Rénale, Paris, France; Université Pierre et Marie Curie, Sorbonne Universités, Paris, France.
Abstract:
Renal epithelial cells arise during embryogenesis by mesenchymal to epithelial transition (MET). In the context of renal diseases, these cells can switch back to a mesenchymal phenotype, in a process thus reminiscent of an epithelial-to-mesenchymal transition (EMT) in which we referred to as "Epithelial Phenotypic Changes" (EPC). The pathophysiological consequence of EPC is controversial: in particular, to what extent EPC contribute to the pool of disease-associated renal fibroblasts is very uncertain. However, there is strong evidence that EPC correlate with a poor renal outcome. EPC indeed reflect an exposure to a profibrotic environment, at an early and potentially reversible stage. Detecting EPC has potential therapeutic implications for patients prone to renal fibrosis, both as a marker of efficacy or more directly as a target. In opposition to the EMT occurring during embryogenesis, EMT in fibrosis as well as in cancer is an anarchic cellular process actually developing at the expense of the whole organ(ism).
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