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Background  The dynamic process of epithelial-to-mesenchymal transition (EMT) is a causal event in kidney fibrosis. This cellular phenotypic transition involves activation of transcriptional responses and remodeling of cellular structures to change cellular function. The molecular mechanisms that directly contribute to the re-establishment of the epithelial phenotype are poorly understood.    Results  Here, we discuss recent studies from our group and other laboratories identifying signaling pathways leading to the reversal of EMT in fibrotic models. We also present evidence that transcriptional factors such as the ZEB proteins are important regulators for reversal of EMT.    Conclusion  These studies provide insights into cellular plasticity and possible targets for therapeutic intervention.

Reversal of transforming growth factor-β induced epithelial-to-mesenchymal transition and the ZEB proteins