Abstract
Introduction and Aim: Non-alcoholic fatty liver disease (NAFLD) heritability is estimated to be within 25-75% and PNPLA3 rs738409 C>G p.I148M variant accounts for a large fraction of disease susceptibility. The p.I148M variant promotes intrahepatic lipid accumulation, progression to cirrhosis and hepatocellular carcinoma. A comprehensive human model to study the role and mechanisms of genetic variability in liver disease is still lacking. Aim of this study is to generate patient-derived human liver organoids (HLOs) to clarify the impact and role of PNPLA3 mutation in NAFLD onset and progression.
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