TY - JOUR
T1 - Hepatocyte specific deletion of c-Met leads to the development of severe non-alcoholic-steatohepatitis in mice
AU - Kroy, Daniela C
AU - Schumacher, Fabienne
AU - Ramadori, Pierluigi
AU - Hatting, Maximilian
AU - Bergheim, Ina
AU - Gassler, Nikolaus
AU - Boekschoten, Mark V
AU - Müller, Michael
AU - Streetz, Konrad L
AU - Trautwein, Christian
N1 - Copyright © 2014. Published by Elsevier B.V.
PY - 2014/10
Y1 - 2014/10
N2 - 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.
AB - 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.
U2 - 10.1016/j.jhep.2014.05.019
DO - 10.1016/j.jhep.2014.05.019
M3 - Article
C2 - 24845607
VL - 61
SP - 883
EP - 890
JO - Journal of Hepatology
JF - Journal of Hepatology
SN - 0168-8278
IS - 4
ER -