A mouse model of alcoholic liver fibrosis-associated acute kidney injury identifies key molecular pathways.

ABSTRACT: Clinical data strongly indicate that acute kidney injury (AKI) is a critical complication in alcoholic hepatitis, an acute-on-chronic form of liver failure in patients with advanced alcoholic fibrosis. Development of targeted therapies for AKI in this setting is hampered by the lack of an animal model. To enable research into molecular drivers and novel therapies for fibrosis- and alcohol-associated AKI, we aimed to combine carbon tetrachloride (CCl₄)-induced fibrosis with chronic intra-gastric alcohol feeding. Male C57BL/6J mice were administered a low dose of CCl₄ (0.2ml/kg 2× week/6weeks) followed by alcohol intragastrically (up to 25g/kg/day for 3weeks) and with continued CCl₄. We observed that combined treatment with CCl₄ and alcohol resulte

SUBMITTER: Furuya S 

PROVIDER: S-EPMC5323078 | biostudies-literature | 2016 Nov

REPOSITORIES: biostudies-literature