从肝纤维化发展为肝硬化和肝细胞癌的血管生成

StephenW

Angiogenesis in the progression from liver fibrosis to cirrhosis and hepatocelluar carcinoma
Hui Li
Pages 217-233 | Received 01 Jun 2020, Accepted 23 Oct 2020, Accepted author version posted online: 31 Oct 2020, Published online: 11 Nov 2020

    Download citation https://doi.org/10.1080/17474124.2021.1842732 CrossMark Logo CrossMark

ABSTRACT

Introduction: Persistent inflammation and hypoxia are strong stimulus for pathological angiogenesis and vascular remodeling, and are also the most important elements resulting in liver fibrosis. Sustained inflammatory process stimulates fibrosis to the end-point of cirrhosis and sinusoidal portal hypertension is an important feature of cirrhosis. Neovascularization plays a pivotal role in collateral circulation formation of portal vein, mesenteric congestion, and high perfusion. Imbalance of hepatic artery and portal vein blood flow leads to the increase of hepatic artery inflow, which is beneficial to the formation of nodules. Angiogenesis contributes to progression from liver fibrosis to cirrhosis and hepatocellular carcinoma (HCC) and anti-angiogenesis therapy can improve liver fibrosis, reduce portal pressure, and prolong overall survival of patients with HCC.

Areas covers: This paper will try to address the difference of the morphological characteristics and mechanisms of neovascularization in the process from liver fibrosis to cirrhosis and HCC and further compare the different efficacy of anti-angiogenesis therapy in these three stages.

Expert opinion: More in-depth understanding of the role of angiogenesis factors and the relationship between angiogenesis and other aspects of the pathogenesis and transformation may be the key to enabling future progress in the treatment of patients with liver fibrosis, cirrhosis, and HCC.

StephenW

从肝纤维化发展为肝硬化和肝细胞癌的血管生成
李慧
第217-233页|于2020年6月1日接收，于2020年10月23日接受，在线接受作者版本：2020年10月31日，在线发布：2020年11月11日

    下载引文https://doi.org/10.1080/17474124.2021.1842732 CrossMark徽标CrossMark

抽象的

简介：持续性炎症和缺氧是病理性血管生成和血管重塑的强烈刺激因素，也是导致肝纤维化的最重要因素。持续的炎症过程将纤维化刺激至肝硬化的终点，而正弦门脉高压是肝硬化的重要特征。新血管形成在门静脉侧支循环形成，肠系膜充血和高灌注中起关键作用。肝动脉和门静脉血流量的不平衡导致肝动脉流入的增加，这有利于结节的形成。血管生成有助于从肝纤维化发展为肝硬化和肝细胞癌（HCC），抗血管生成治疗可以改善肝纤维化，降低门脉压力并延长HCC患者的总体生存期。

领域涵盖：本文将试图探讨从肝纤维化到肝硬化和肝癌的过程中新血管形成的形态学特征和机制的差异，并进一步比较这三个阶段抗血管生成治疗的不同疗效。

专家意见：对血管生成因子的作用以及血管生成与发病机理和转化其他方面之间的关系的更深入了解，可能是使肝纤维化，肝硬化和HCC患者治疗取得新进展的关键。