Hypoxia,angiogenesis and liver fibrogenesis in the progression of chronic liver diseases

作     者：Claudia Paternostro Ezio David Erica Novo Maurizio Parola 

作者机构：Department of Experimental Medicine and OncologyInteruniversity Centre for Hepatic PathophysiologyUniversity of Torino Department of PathologySan Giovanni Battista Hospital 

出 版 物：《World Journal of Gastroenterology》 (世界胃肠病学杂志（英文版）)

年 卷 期：2010年第16卷第3期

页      面：281-288页

核心收录：

学科分类：1002[医学-临床医学] 100201[医学-内科学(含：心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学] 

主　　题：Chronic liver diseases Hepatic myofi broblasts Hypoxia Liver angiogenesis Liver fi brogenesis 

摘      要：Angiogenesis is a dynamic,hypoxia-stimulated and growth factor-dependent process,and is currently referred to as the formation of new vessels from preexisting blood *** and clinical studies have unequivocally reported that hepatic angiogenesis,irrespective of aetiology,occurs in conditions of chronic liver diseases(CLDs) characterized by perpetuation of cell injury and death,inflammatory response and progressive *** and related changes in liver vascular architecture,that in turn concur to increase vascular resistance and portal hypertension and to decrease parenchymal perfusion,have been proposed to favour fibrogenic progression of the disease towards the end-point of ***,hepatic angiogenesis has also been proposed to modulate the genesis of portal-systemic shunts and increase splanchnic blood flow,thus potentially affecting complications of *** angiogenesis is also crucial for the growth and progression of hepatocellular *** literature has identified a number of cellular and molecular mechanisms governing the cross-talk between angiogenesis and fibrogenesis,with a specifi c emphasis on the crucial role of hypoxic conditions and hepatic stellate cells,particularly when activated to the myofibroblast-like *** anti-angiogenic therapy has been proven to be effective in limiting the progression of CLDs in animal *** a clinical point of view,anti-angiogenic therapy is currently emerging as a new pharmacologic intervention in patients with advanced fibrosis and cirrhosis.