Brain Arteriovenous Malformation Modeling, Pathogenesis, and Novel Therapeutic Targets

被引：49

作者：

Chen, Wanqiu ^{[1
]}

Choi, Eun-Jung ^{[1
]}

McDougall, Cameron M. ^{[1
]}

Su, Hua ^{[1
]}

机构：

[1] Univ Calif San Francisco, Ctr Cerebrovasc Res, Dept Anesthesia & Perioperat Care, San Francisco, CA 94110 USA

来源：

TRANSLATIONAL STROKE RESEARCH | 2014年 / 5卷 / 03期

基金：

美国国家卫生研究院;

关键词：

Activin-like kinase 1; Angiogenesis; Brain arteriovenous malformation; Conditional knockout; Endoglin; Hereditary hemorrhagic telangiectasia; Mouse models; HEREDITARY HEMORRHAGIC TELANGIECTASIA; ENDOTHELIAL GROWTH-FACTOR; CAUSE CEREBROVASCULAR DYSPLASIA; HYPOXIA-INDUCIBLE FACTOR; MATRIX METALLOPROTEINASES; MOUSE MODEL; INTRACRANIAL HEMORRHAGE; VASCULAR MALFORMATIONS; ADULT-MOUSE; BONE-MARROW;

D O I：

10.1007/s12975-014-0343-0

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

Patients harboring brain arteriovenous malformation (bAVM) are at life-threatening risk of rupture and intracranial hemorrhage (ICH). The pathogenesis of bAVM has not been completely understood. Current treatment options are invasive, and a parts per thousand 20 % of patients are not offered interventional therapy because of excessive treatment risk. There are no specific medical therapies to treat bAVMs. The lack of validated animal models has been an obstacle for testing hypotheses of bAVM pathogenesis and testing new therapies. In this review, we summarize bAVM model development and bAVM pathogenesis and potential therapeutic targets that have been identified during model development.

引用

页码：316 / 329

页数：14

共 172 条

[1] Association of tumor necrosis factor-α-238G>A and apolipoprotein E2 polymorphisms with intracranial hemorrhage after brain artericivenous malformation treatment [J].