title: Embolization-induced angiogenesis in cerebral arteriovenous malformations.
abstract: 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.
authors.affiliation: University of Virginia, Department of Neurosurgery, P.O. Box 800212, Charlottesville, VA 22908, USA. Electronic address: tjb4p@hscmail.mcc.virginia.edu.
authors.forename: Thomas J
authors.initials: TJ
authors.lastname: Buell
authors.affiliation: University of Virginia, Department of Neurosurgery, P.O. Box 800212, Charlottesville, VA 22908, USA.
authors.forename: Dale
authors.initials: D
authors.lastname: Ding
authors.affiliation: University of Virginia, Department of Neurosurgery, P.O. Box 800212, Charlottesville, VA 22908, USA.
authors.forename: Robert M
authors.initials: RM
authors.lastname: Starke
authors.affiliation: University of Virginia, Department of Neurosurgery, P.O. Box 800212, Charlottesville, VA 22908, USA.
authors.forename: R
authors.initials: R
authors.lastname: Webster Crowley
authors.affiliation: University of Virginia, Department of Neurosurgery, P.O. Box 800212, Charlottesville, VA 22908, USA.
authors.forename: Kenneth C
authors.initials: KC
authors.lastname: Liu
mesh_terms: D015703:Antigens, CD / Q000502:physiology; D015687:Cell Hypoxia; D002560:Cerebrovascular Circulation; D003131:Combined Modality Therapy; D004121:Dimethyl Sulfoxide / Q000528:radiation effects / Q000627:therapeutic use; D004621:Embolization, Therapeutic / Q000009:adverse effects*; D000071063:Endoglin; D005544:Forecasting; D005786:Gene Expression Regulation; D006439:Hemodynamics; D006801:Humans; D007249:Inflammation; D002538:Intracranial Arteriovenous Malformations / Q000150:complications / Q000601:surgery / Q000628:therapy*; D008955:Models, Cardiovascular; D009389:Neovascularization, Pathologic / Q000209:etiology* / Q000503:physiopathology / Q000517:prevention & control; D011145:Polyvinyls / Q000528:radiation effects / Q000627:therapeutic use; D016634:Radiosurgery; D011956:Receptors, Cell Surface / Q000502:physiology; D020521:Stroke / Q000209:etiology / Q000517:prevention & control; D016896:Treatment Outcome; D042461:Vascular Endothelial Growth Factor A / Q000037:antagonists & inhibitors / Q000096:biosynthesis / Q000235:genetics; D040301:Vascular Endothelial Growth Factor Receptor-2 / Q000502:physiology
chemical_list: D015703:Antigens, CD; C064206:ENG protein, human; D000071063:Endoglin; C450660:Onyx copolymer; D011145:Polyvinyls; D011956:Receptors, Cell Surface; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D040301:Vascular Endothelial Growth Factor Receptor-2; D004121:Dimethyl Sulfoxide
keywords: Angiogenesis; Arteriovenous malformation; Embolization; Hypoxia; Inflammation; Stroke