Embolization-induced angiogenesis in cerebral arteriovenous malformations

被引:101
作者
Buell, Thomas J. [1 ]
Ding, Dale [1 ]
Starke, Robert M. [1 ]
Crowley, R. Webster [1 ]
Liu, Kenneth C. [1 ]
机构
[1] Univ Virginia, Dept Neurosurg, Charlottesville, VA 22908 USA
关键词
Angiogenesis; Arteriovenous malformation; Embolization; Hypoxia; Inflammation; Stroke; ENDOTHELIAL GROWTH-FACTOR; SMOOTH-MUSCLE-CELLS; VASCULAR MALFORMATIONS; CLINICAL ARTICLE; STEREOTACTIC RADIOSURGERY; SHEAR-STRESS; ADULT-MOUSE; LONG-TERM; FOLLOW-UP; BRAIN;
D O I
10.1016/j.jocn.2014.04.010
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Endovascular occlusion of cerebral arteriovenous malformations (AVM) is often utilized as adjunctive therapy in combination with radiosurgery or microsurgery. Evidence supports that partial occlusion of AVM via endovascular embolization leads to increased angiogenesis. This phenomenon may be a contributing factor to the decreased efficacy of AVM radiosurgery following embolization. We review the literature for potential mechanisms of embolization-induced angiogenesis. A comprehensive literature search was performed using PubMed to identify studies that sought to elucidate the pathophysiology behind embolization-induced angiogenesis. The terms "arteriovenous malformation", "embolization", and "angiogenesis" were used to search for relevant publications individually and together. Three distinct mechanisms for embolization-induced angiogenesis were described in the literature: (1) hypoxia-mediated angiogenesis, (2) inflammatory-mediated angiogenesis, and (3) hemodynamic-mediated angiogenesis. Embolization-induced angiogenesis of cerebral AVM likely results from a combination of the three aforementioned mechanisms. However, future research is necessary to determine the relative contribution of each individual mechanism to overall post-embolization AVM neovascularization. (C) 2014 Elsevier Ltd. All rights reserved.
引用
收藏
页码:1866 / 1871
页数:6
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