Mice lacking liver-specific β-catenin develop steatohepatitis and fibrosis after iron overload.

ABSTRACT:

Background & aims

Iron overload disorders such as hereditary hemochromatosis and iron loading anemias are a common cause of morbidity from liver diseases and increase risk of hepatic fibrosis and hepatocellular carcinoma (HCC). Treatment options for iron-induced damage are limited, partly because there is lack of animal models of human disease. Therefore, we investigated the effect of iron overload in liver-specific β-catenin knockout mice (KO), which are susceptible to injury, fibrosis and tumorigenesis following chemical carcinogen exposure.

Methods

Iron overload diet was administered to KO and littermate control (CON) mice for various times. To ameliorate an oxidant-mediated component of tissue injury, N-Acetyl-L-(+)-cysteine (NAC) was added to drinking water of mice on i

SUBMITTER: Preziosi ME 

PROVIDER: S-EPMC5515705 | biostudies-literature | 2017 Aug

REPOSITORIES: biostudies-literature