Evidence of cell-fate conversion from hepatocytes to cholangiocytes in the injured liver: in-vivo genetic lineage-tracing approachesSuzuki, Atsushia,bCurrent Opinion in Gastroenterology: May 2015 - Volume 31 - Issue 3 - p 247–251 doi: 10.1097/MOG.0000000000000172 BILIARY TRACT: Edited by Gregory J. Gores Abstract Author Information Purpose of review Recently, it has been suggested that hepatocytes can potentially convert their fate into that of cholangiocytes when the liver receives an injury. This review concisely summarizes these new findings, especially those obtained in studies using cell-lineage tracing methods. Recent findings Recent advances in technologies using mutant mice with a tamoxifen-inducible Cre/loxP system have allowed heritable labeling of a particular type of cell and enabled us to follow the fate of their progeny. This is generally known as ‘genetic lineage-tracing’, and has been applied in various studies that require tracking of the fate of cells in living mice. Previous studies using these methods have revealed that hepatocytes themselves can give rise to cholangiocytes through Notch-mediated cell-fate conversion from hepatocytes to cholangiocytes in injured liver tissue and at the onset of liver cancer. Summary Intensive studies using in-vivo genetic lineage-tracing approaches have provided new insights into the nature of cellular identity and plasticity in the liver, which will contribute to the development of new therapeutic strategies for liver diseases. aDivision of Organogenesis and Regeneration, Medical Institute of Bioregulation, Kyushu University, Fukuoka bCore Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency, Saitama, Japan Correspondence to Atsushi Suzuki, Division of Organogenesis and Regeneration, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan. Tel: +81 92 642 6793; fax: +81 92 642 6793; e-mail: email@example.com Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.