Hepatocyte specific deletion of c-Met leads to the development of severe non-alcoholic-steatohepatitis in mice

Daniela C Kroy, Fabienne Schumacher, Pierluigi Ramadori, Maximilian Hatting, Ina Bergheim, Nikolaus Gassler, Mark V Boekschoten, Michael Müller, Konrad L Streetz, Christian Trautwein

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Abstract

Non-alcoholic-fatty-liver disease (NAFLD) is part of the metabolic syndrome. The spectrum of NAFLD includes NASH (non-alcoholic steatohepatitis), which is characterized by progressive inflammation associated with oxidative stress and apoptosis finally triggering liver cirrhosis and hepatocellular carcinoma. HGF (hepatocyte growth factor)/mesenchymal-epithelial transition factor (c-Met) receptor signaling is known to activate distinct intracellular pathways mediating among others anti-apoptotic properties to hepatocytes. Therefore, the aim was to characterize the role of c-met during NASH development.
Original languageEnglish
Pages (from-to)883–890
Number of pages8
JournalJournal of Hepatology
Volume61
Issue number4
Early online date15 May 2014
DOIs
Publication statusPublished - Oct 2014

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