Role of Angiogenesis in the Pathogenesis of NAFLD

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.

Automated summary

Non-alcoholic fatty liver disease (NAFLD) is associated with liver angiogenesis, which may lead to liver fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). Research has shown that angiogenesis plays a crucial role in the progression of NAFLD, and targeting angiogenesis, particularly VEGF, could be a potential treatment for NAFLD.