P28 PD Dr. Strnad
Iron and α1-antitrypsin accumulation as hepatocellular initiators of liver fibrosis

We aim to analyze the role of iron overload and α1-antitrypsin (AAT) mutation as human-relevant models of liver fibrosis initiation. The impact of lysosomal dysfunction will be assessed in hepcidin knockout (KOs, iron overload model) and AAT mutated animals cross-bred with p62 KO or CHOP KO mice. Animal studies will be complemented by evaluation of AAT patients in order to define mechanisms of disease development and the role of co-founding factors such as obesity and alcohol consumption.