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本文引用的文献

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H3 histamine receptor-mediated activation of protein kinase Calpha inhibits the growth of cholangiocarcinoma in vitro and in vivo.H3 组氨酸受体介导致蛋白激酶 Calpha 的激活抑制胆管癌细胞在体外和体内的生长。
Mol Cancer Res. 2009 Oct;7(10):1704-13. doi: 10.1158/1541-7786.MCR-09-0261. Epub 2009 Oct 13.
2
ERK1/2-dependent vascular endothelial growth factor signaling sustains cyst growth in polycystin-2 defective mice.ERK1/2 依赖性血管内皮生长因子信号维持多囊蛋白-2 缺陷小鼠的囊肿生长。
Gastroenterology. 2010 Jan;138(1):360-371.e7. doi: 10.1053/j.gastro.2009.09.005. Epub 2009 Sep 18.
3
Pharmacological inhibition of integrin alphavbeta3 aggravates experimental liver fibrosis and suppresses hepatic angiogenesis.整合素αvβ3的药理学抑制作用会加重实验性肝纤维化并抑制肝血管生成。
Hepatology. 2009 Nov;50(5):1501-11. doi: 10.1002/hep.23144.
4
Genetic variation in the vascular endothelial growth factor gene is associated with biliary atresia.血管内皮生长因子基因的遗传变异与胆道闭锁有关。
J Clin Gastroenterol. 2010 Feb;44(2):135-9. doi: 10.1097/MCG.0b013e3181b152c2.
5
Liver cyst cytokines promote endothelial cell proliferation and development.肝囊肿细胞因子促进内皮细胞增殖和发育。
Exp Biol Med (Maywood). 2009 Oct;234(10):1155-65. doi: 10.3181/0903-RM-112. Epub 2009 Jul 13.
6
Repair-related activation of hedgehog signaling promotes cholangiocyte chemokine production.与修复相关的刺猬信号通路激活促进胆管细胞趋化因子的产生。
Hepatology. 2009 Aug;50(2):518-27. doi: 10.1002/hep.23019.
7
The function of vascular endothelial growth factor.血管内皮生长因子的功能。
Biofactors. 2009 Jul-Aug;35(4):332-7. doi: 10.1002/biof.46.
8
Vandetanib (ZD6474), an inhibitor of VEGFR and EGFR signalling, as a novel molecular-targeted therapy against cholangiocarcinoma.凡德他尼(ZD6474),一种VEGFR和EGFR信号通路抑制剂,作为一种针对胆管癌的新型分子靶向疗法。
Br J Cancer. 2009 Apr 21;100(8):1257-66. doi: 10.1038/sj.bjc.6604988. Epub 2009 Mar 24.
9
Endothelin inhibits cholangiocarcinoma growth by a decrease in the vascular endothelial growth factor expression.内皮素通过降低血管内皮生长因子的表达来抑制胆管癌生长。
Liver Int. 2009 Aug;29(7):1031-42. doi: 10.1111/j.1478-3231.2009.01997.x. Epub 2009 Mar 9.
10
Taurocholate feeding to bile duct ligated rats prevents caffeic acid-induced bile duct damage by changes in cholangiocyte VEGF expression.给胆管结扎大鼠喂食牛磺胆酸盐可通过改变胆管上皮细胞血管内皮生长因子(VEGF)的表达来预防咖啡酸诱导的胆管损伤。
Exp Biol Med (Maywood). 2009 Apr;234(4):462-74. doi: 10.3181/0808-RM-255. Epub 2009 Feb 20.

血管因素、血管生成与胆道疾病。

Vascular factors, angiogenesis and biliary tract disease.

机构信息

Scott & White Digestive Disease Research Center, Department of Medicine, Division Gastroenterology, Texas A&M Health Science Center, Temple, Texas, USA.

出版信息

Curr Opin Gastroenterol. 2010 May;26(3):246-50. doi: 10.1097/MOG.0b013e3283369d19.

DOI:10.1097/MOG.0b013e3283369d19
PMID:20061944
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2893138/
Abstract

PURPOSE OF REVIEW

Recent studies have brought to light that angiogenesis and the expression of pro-angiogenic factors such as vascular endothelial growth factors (VEGFs) participate in the pathogenesis of biliary tract diseases. This review summarizes recent progress that has been accomplished in the field, which expands our understanding of the relationship between vascular growth and the biliary tract, particularly the molecular mechanisms that underlie the pathogenesis of biliary tract diseases.

RECENT FINDINGS

Angiogenesis and the expression of vascular factors play a key role in the pathogenesis of primary biliary cirrhosis, cholangiocarcinoma, liver cysts, and in the progression of biliary fibrosis in animal models. Inhibition of angiogenesis limits fibrosis in animal models, whereas the bile acid, taurocholate, has protective effects in animal models of bile duct and peribiliary vascular plexus damage.

SUMMARY

A widening body of information indicates that the expression of pro-angiogenic factors such as VEGFs and angiogenesis play an important role in a variety of biliary tract diseases. Further characterization of the link between angiogenesis and vascular growth factor expression will help in elucidating the mechanisms regulating the pathogenesis of biliary tract diseases and in devising new treatment approaches for these devastating diseases.

摘要

目的综述

最近的研究表明,血管生成和促血管生成因子(如血管内皮生长因子 [VEGFs])的表达参与了胆道疾病的发病机制。本综述总结了该领域最近取得的进展,这些进展扩展了我们对血管生长与胆道之间关系的理解,特别是对胆道疾病发病机制的分子机制的理解。

最近的发现

血管生成和血管因子的表达在原发性胆汁性肝硬化、胆管癌、肝囊肿以及动物模型中的胆道纤维化进展中起着关键作用。在动物模型中,抑制血管生成可限制纤维化,而胆酸牛磺胆酸盐在胆管和胆周血管丛损伤的动物模型中具有保护作用。

总结

越来越多的信息表明,促血管生成因子如 VEGFs 的表达和血管生成在多种胆道疾病中起着重要作用。进一步阐明血管生成与血管生长因子表达之间的联系将有助于阐明调节胆道疾病发病机制的机制,并为这些破坏性疾病设计新的治疗方法。