ECE2021 Audio Eposter Presentations Diabetes, Obesity, Metabolism and Nutrition (223 abstracts)
1CiMUS, Department of Physiology, University of Santiago de Compostela, Spain; 2CIC BioGUNE, Spain; 3Centro Nacional de Investigaciones Cardiovasculares Carlos III, Spain; 4Servicio de Medicina Interna. Hospital Universitario de Salamanca, Spain
p53 family controls several metabolic and cellular functions. The p63 member regulates lipid metabolism in hepatocytes and contributes to the development of liver steatosis. Here we show that p63 plays an important role in liver fibrosis. P63 is upregulated in patients with NASH, correlating positively with fibrosis score and collagen 1a1 expression. P63 expression is also increased in different animal models of diet-induced NASH and chemically induced liver fibrosis. Mice with hepatic downregulation of p63 fed a high fat diet or choline deficient and high fat diet (CDHFD) for 52 weeks display reduced collagen deposition, hydroxyproline levels and expression of collagen markers. Similar results were found when these mice were challenged to methionine and choline deficient diet. Consistent with this, the hepatic overexpression of TAp63α isoform accelerates the fibrosis induced by CDHFD. Our findings indicate an unexpected role of p63 in the metabolic and profibrotic action in liver disease.