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Abstract Details
Role of Angiogenesis in the Pathogenesis of NAFLD
J Clin Med. 2021 Mar 24;10(7):1338. doi: 10.3390/jcm10071338.
Lin Lei1, Haquima Ei Mourabit1, Chantal Housset12, Axelle Cadoret1, Sara Lemoinne12
Author information
1Centre de Recherche Saint-Antoine (CRSA) and Institute of Cardiometabolism and Nutrition (ICAN), Sorbonne Université, INSERM, 75012 Paris, France.
2Department of Hepatology, Reference Center for Inflammatory Biliary Diseases and Autoimmune Hepatitis (CRMR, MIVB-H), Assistance Publique-Hôpitaux de Paris (AP-HP), Saint-Antoine Hospital, 75012 Paris, France.
Abstract
Non-alcoholic fatty liver disease (NAFLD) has become the leading cause of chronic liver disease, exposing to the risk of liver fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). Angio-genesis is a complex process leading to the development of new vessels from pre-existing vessels. Angiogenesis is triggered by hypoxia and inflammation and is driven by the action of proangiogenic cytokines, mainly vascular endothelial growth factor (VEGF). In this review, we focus on liver angiogenesis associated with NAFLD and analyze the evidence of liver angiogenesis in animal models of NAFLD and in NAFLD patients. We also report the data explaining the role of angiogenesis in the progression of NAFLD and discuss the potential of targeting angiogenesis, notably VEGF, to treat NAFLD.