Paola Berenice Mass-Sanchez, Marinela Krizanac, Paula Štancl, Marvin Leopold, Kathrin M Engel, Eva Miriam Buhl, Josef van Helden, Nikolaus Gassler, Jürgen Schiller, Rosa Karlić, Diana Möckel, Twan Lammers, Steffen K Meurer, Ralf Weiskirchen, Anastasia Asimakopoulos
The molecular mechanisms underlying the transition from nonalcoholic fatty liver disease (NAFLD) to hepatocellular carcinoma (HCC) are incompletely understood. During the development of NAFLD, Perilipin 5 (PLIN5) can regulate lipid metabolism by suppressing lipolysis and preventing lipotoxicity. Other reports suggest that the lack of PLIN5 decreases hepatic injury, indicating a protective role in NAFLD pathology. To better understand the role of PLIN5 in liver disease, we established mouse models of NAFLD and NAFLD-induced HCC, in which wild-type and Plin5 null mice were exposed to a single dose of acetone or 7,12-dimethylbenz[a]anthracene (DMBA) in acetone, followed by a 30-week high-fat diet supplemented with glucose/fructose...
February 22, 2024: Cell Death Discovery