| Literature DB >> 23612071 |
Pierre Galichon1, Serge Finianos, Alexandre Hertig.
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).Entities:
Keywords: Alk3; BMP; EMT; Epithelial to mesenchymal transition; FSP1; Fibrosis; HGF; HSP72; IRI; Ilk; Kidney; NTN; STZ; TEC; TGFβ; Tubular epithelial cell; UUO; activin-like kinase 3, a BMP receptor; alpha smooth muscle actin; bone morphogenetic protein; epithelial–mesenchymal transition; fibroblast specific protein 1; heat shock protein; hepatocyte growth factor; integrin-linked kinase; ischemia-reperfusion injury; nephrotoxic serum nephritis; recombinant human; rh; streptozotocin (a toxic compound that produces pancreatic injury and diabetes); transforming growth factor beta; tubular epithelial cells; unilateral ureteral obstruction; α-SMA
Mesh:
Year: 2013 PMID: 23612071 DOI: 10.1016/j.canlet.2013.04.018
Source DB: PubMed Journal: Cancer Lett ISSN: 0304-3835 Impact factor: 8.679