血管生成在肝硬化门脉高压(PHT)中的研究进展

 门脉高压(portal hypertension,PHT)是慢性肝病肝硬化患者主要的并发症之一,近年来,新生血管形成在PHT中的作用受到越来越多学者的关注。病理性血管生成早在肝硬化及RHT形成之前就已发生,是疾病进展的重要环节。PHT病理性血管生成的机制包括缺氧及炎症反应、细胞间的信号传导及相互作用、血管内皮基因表型改变等,本文将主要阐述这3个方面的机制以及血管抑制生成的药物研究进展。

Advance in the role of angiogenesis in the progression of portal hypertension (PHT) caused by cirrhosis

Portal hypertension (PHT) is one of the most important complications of liver cirrhosis in patients with chronic hepatdogic diseases.Recently the effect of angiogenesis on PHT is the hotpoint in current studies.Pathologic angiogenesis occures before liver cirrhosis and PHT,which also plays an critical role in aggravating the PHT,which triggered by hypoxia,cell cell crosstalk and endothelial genetic change.So we mainly review the three ways that induces angiogenesis and the newly discovered anti angiogenesis drugs.