Hepcidin knockout mice as a model of iron-overload associated liver disease

Background and aims: Hepcidin is the central regulator of iron homeostasis. Disrupted hepcidin signalling results in hereditary hemochromatosis and iron overload in chronic liver disorders. While the association between iron overload and development of end-stage liver disease is well established, our understanding of the underlying pathomechanisms is hampered by the lack of a suitable animal model. To circumvent this problem, we studied hepcidin-knockout (KO) mice as a model of iron-overload associated liver damage. Methods: 6 month-old hepcidin-KO and -wild type (WT) mice fed 3% iron carbonyl-containing diet (F…