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Biology of cerebral arteriovenous malformations with a focus on inflammation.

Publication ,  Journal Article
Mouchtouris, N; Jabbour, PM; Starke, RM; Hasan, DM; Zanaty, M; Theofanis, T; Ding, D; Tjoumakaris, SI; Dumont, AS; Ghobrial, GM; Kung, D ...
Published in: J Cereb Blood Flow Metab
February 2015

Cerebral arteriovenous malformations (AVMs) entail a significant risk of intracerebral hemorrhage owing to the direct shunting of arterial blood into the venous vasculature without the dissipation of the arterial blood pressure. The mechanisms involved in the growth, progression and rupture of AVMs are not clearly understood, but a number of studies point to inflammation as a major contributor to their pathogenesis. The upregulation of proinflammatory cytokines induces the overexpression of cell adhesion molecules in AVM endothelial cells, resulting in enhanced recruitment of leukocytes. The increased leukocyte-derived release of metalloproteinase-9 is known to damage AVM walls and lead to rupture. Inflammation is also involved in altering the AVM angioarchitecture via the upregulation of angiogenic factors that affect endothelial cell proliferation, migration and apoptosis. The effects of inflammation on AVM pathogenesis are potentiated by certain single-nucleotide polymorphisms in the genes of proinflammatory cytokines, increasing their protein levels in the AVM tissue. Furthermore, studies on metalloproteinase-9 inhibitors and on the involvement of Notch signaling in AVMs provide promising data for a potential basis for pharmacological treatment of AVMs. Potential therapeutic targets and areas requiring further investigation are highlighted.

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Published In

J Cereb Blood Flow Metab

DOI

EISSN

1559-7016

Publication Date

February 2015

Volume

35

Issue

2

Start / End Page

167 / 175

Location

United States

Related Subject Headings

  • Up-Regulation
  • Signal Transduction
  • Receptors, Notch
  • Polymorphism, Single Nucleotide
  • Neurology & Neurosurgery
  • Matrix Metalloproteinase 9
  • Leukocytes
  • Intracranial Arteriovenous Malformations
  • Inflammation
  • Humans
 

Citation

APA
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ICMJE
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Mouchtouris, N., Jabbour, P. M., Starke, R. M., Hasan, D. M., Zanaty, M., Theofanis, T., … Chalouhi, N. (2015). Biology of cerebral arteriovenous malformations with a focus on inflammation. J Cereb Blood Flow Metab, 35(2), 167–175. https://doi.org/10.1038/jcbfm.2014.179
Mouchtouris, Nikolaos, Pascal M. Jabbour, Robert M. Starke, David M. Hasan, Mario Zanaty, Thana Theofanis, Dale Ding, et al. “Biology of cerebral arteriovenous malformations with a focus on inflammation.J Cereb Blood Flow Metab 35, no. 2 (February 2015): 167–75. https://doi.org/10.1038/jcbfm.2014.179.
Mouchtouris N, Jabbour PM, Starke RM, Hasan DM, Zanaty M, Theofanis T, et al. Biology of cerebral arteriovenous malformations with a focus on inflammation. J Cereb Blood Flow Metab. 2015 Feb;35(2):167–75.
Mouchtouris, Nikolaos, et al. “Biology of cerebral arteriovenous malformations with a focus on inflammation.J Cereb Blood Flow Metab, vol. 35, no. 2, Feb. 2015, pp. 167–75. Pubmed, doi:10.1038/jcbfm.2014.179.
Mouchtouris N, Jabbour PM, Starke RM, Hasan DM, Zanaty M, Theofanis T, Ding D, Tjoumakaris SI, Dumont AS, Ghobrial GM, Kung D, Rosenwasser RH, Chalouhi N. Biology of cerebral arteriovenous malformations with a focus on inflammation. J Cereb Blood Flow Metab. 2015 Feb;35(2):167–175.
Journal cover image

Published In

J Cereb Blood Flow Metab

DOI

EISSN

1559-7016

Publication Date

February 2015

Volume

35

Issue

2

Start / End Page

167 / 175

Location

United States

Related Subject Headings

  • Up-Regulation
  • Signal Transduction
  • Receptors, Notch
  • Polymorphism, Single Nucleotide
  • Neurology & Neurosurgery
  • Matrix Metalloproteinase 9
  • Leukocytes
  • Intracranial Arteriovenous Malformations
  • Inflammation
  • Humans