Pathological Angiogenesis: The New Culprit behind Chronic Liver Disease

Abstract

Angiogenesis is the formation of new blood vessels from the existing ones. It is a complex and highly regulated process which plays a role in a wide variety of physiological and pathological processes. Angiogenesis is essential for a variety of functions in chronic liver disease, including the development and establishment of liver inflammation and fibrosis, the formation of portosystemic collaterals, increase in the splanchnic blood flow, and portal hypertension. Angiogenesis involves a sequence of well-coordinated events which are mediated by a number of strictly regulated interactions between the pro-angiogenic factors and their corresponding receptors expressed on the surface of various vascular (e.g., endothelial cells and pericytes) and stromal components constituting the extracellular matrix. The present review provides an overview of the contribution of angiogenesis to the progression of chronic liver disease, and discusses the functional roles of the key growth factors and cytokines that are known to promote angiogenesis in liver disease, including the vascular endothelial growth factor, placental growth factor, platelet-derived endothelial cell growth factor, and the angiopoietin system. Inhibiting the activity of the aforementioned

HCV and HCC Tango—Deciphering the Intricate Dance of Disease: A Review Article

“…Hypoxia, oxidative stress, inflammation, and impaired endothelial function can potentially trigger the activation of proangiogenic factors. Vascular endothelial growth factor (VEGF), placental growth factor (PlGF), and platelet-derived growth factor (PDGF) induce significant neovascularization within the liver and mesenteric vascular region in the context of cirrhosis [41]. Angiopoietins (Angs) and their corresponding tyrosine kinase receptors are cytokines with proangiogenic properties that are upregulated in liver cirrhosis, impacting prognosis [42].…”