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标题: 從肝纖維化發展為肝硬化和肝細胞癌的血管生成 [打印本页]

作者: StephenW    时间: 2020-11-12 21:03     标题: 從肝纖維化發展為肝硬化和肝細胞癌的血管生成

Angiogenesis in the progression from liver fibrosis to cirrhosis and hepatocelluar carcinoma
Hui Li
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.
KEYWORDS: Angiogenesis, liver fibrosis, liver cirrhosis, HCC, progression

作者: StephenW    时间: 2020-11-12 21:04

從肝纖維化發展為肝硬化和肝細胞癌的血管生成
李慧
於2020年6月1日接收,於2020年10月23日接受,在線接受作者版本:2020年10月31日,在線發布:2020年11月11日

    下載引文https://doi.org/10.1080/17474124.2021.1842732 CrossMark徽標CrossMark

抽象

簡介:持續性炎症和缺氧是病理性血管生成和血管重塑的強烈刺激因素,也是導致肝纖維化的最重要因素。持續的炎症過程將纖維化刺激至肝硬化的終點,而正弦門脈高壓症是肝硬化的重要特徵。新血管形成在門靜脈側支循環形成,腸系膜充血和高灌注中起關鍵作用。肝動脈和門靜脈血流量的不平衡導致肝動脈流入的增加,這有利於結節的形成。血管生成有助於從肝纖維化發展為肝硬化和肝細胞癌(HCC),抗血管生成治療可以改善肝纖維化,降低門脈壓力並延長HCC患者的總體生存期。

領域涵蓋:本文將試圖探討從肝纖維化到肝硬化和肝癌的過程中新血管形成的形態學特徵和機制的差異,並進一步比較這三個階段抗血管生成治療的不同療效。

專家意見:更深入地了解血管生成因子的作用以及血管生成與發病機理和轉化的其他方面之間的關係,可能是在肝纖維化,肝硬化和HCC患者治療方面取得未來進展的關鍵。
關鍵詞:血管生成,肝纖維化,肝硬化,肝癌,進展




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