Hepcidin knockout mice develop chronic liver injury and liver fibrosis as a consequence of lysosomal iron overload

Background and Aims: Hepcidin is the central regulator of iron homeostasis. Disrupted hepcidin signaling results in hereditary hemochromatosis and iron overload seen in chronic liver disorders. While the association between iron overload and development of end-stage liver disease is well established, the understanding of the underlying mechanisms is hampered by the lack of a suitable animal model. To circumvent this problem, we analyzed hepcidin-knockout (KO) mice as a model of iron-overload associated liver disease. Methods: Hepcidin wild-type (WT) and KO animals fed 3% carbonyl iron-containing chow were compar…