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Pathogenesis of Type 2 Epithelial to Mesenchymal Transition (EMT) in Renal and Hepatic Fibrosis

1
Laboratory of Veterinary Pathology, Life and Environmental Sciences, Osaka Prefecture University, Rinkuu Ourai Kita 1-58, Izumisano, Osaka 598-8531, Japan
2
Teaching Hospital Peradeniya, Peradeniya 20400, Sri Lanka
*
Author to whom correspondence should be addressed.
Academic Editors: David A. Brenner, Tatiana Kisseleva and Jonas Fuxe
J. Clin. Med. 2016, 5(1), 4; https://doi.org/10.3390/jcm5010004
Received: 30 November 2015 / Revised: 22 December 2015 / Accepted: 24 December 2015 / Published: 30 December 2015
(This article belongs to the Special Issue Epithelial-Mesenchymal Transition)
Epithelial to mesenchymal transition (EMT), particularly, type 2 EMT, is important in progressive renal and hepatic fibrosis. In this process, incompletely regenerated renal epithelia lose their epithelial characteristics and gain migratory mesenchymal qualities as myofibroblasts. In hepatic fibrosis (importantly, cirrhosis), the process also occurs in injured hepatocytes and hepatic progenitor cells (HPCs), as well as ductular reaction-related bile epithelia. Interestingly, the ductular reaction contributes partly to hepatocarcinogenesis of HPCs, and further, regenerating cholangiocytes after injury may be derived from hepatic stellate cells via mesenchymal to epithelia transition, a reverse phenomenon of type 2 EMT. Possible pathogenesis of type 2 EMT and its differences between renal and hepatic fibrosis are reviewed based on our experimental data. View Full-Text
Keywords: epithelial to mesenchymal transition; renal fibrosis; hepatic fibrosis; animal models; myofibroblasts; hepatic progenitor cells; bile ductular reaction epithelial to mesenchymal transition; renal fibrosis; hepatic fibrosis; animal models; myofibroblasts; hepatic progenitor cells; bile ductular reaction
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Tennakoon, A.H.; Izawa, T.; Kuwamura, M.; Yamate, J. Pathogenesis of Type 2 Epithelial to Mesenchymal Transition (EMT) in Renal and Hepatic Fibrosis. J. Clin. Med. 2016, 5, 4.

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