Persistent mTORC1 activation due to loss of liver tuberous sclerosis complex 1 promotes liver injury in alcoholic hepatitis
Conclusions: Our findings indicate that persistent activation of mTORC1 due to the loss of
cholangiocyte TSC1 promotes liver cell repopulation, ductular reaction, inflammation,
fibrosis, and liver injury in Gao-binge alcohol-fed L-Tsc1 KO mice, which phenocopy the
pathogenesis of human AH.
cholangiocyte TSC1 promotes liver cell repopulation, ductular reaction, inflammation,
fibrosis, and liver injury in Gao-binge alcohol-fed L-Tsc1 KO mice, which phenocopy the
pathogenesis of human AH.