Evidence map›Paper›PMID 25407267›Full record

ReviewJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2015

Biology of cerebral arteriovenous malformations with a focus on inflammation.

Nikolaos Mouchtouris, Pascal M Jabbour, Robert M Starke, David M Hasan, Mario Zanaty, Thana Theofanis, Dale Ding, Stavropoula I Tjoumakaris, Aaron S Dumont, George M Ghobrial and 3 more

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 1 pooled it
11.3field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

55 citing papers in PubMed, 1 synthesis or guideline pooled it, 149 citations in OpenAlex.

  1. Pooled it
  2. A Clinical Feasibility Study to Image Angiogenesis in Patients with Arteriovenous Malformations UsingJournal of nuclear medicine : official publication, Society of Nuclear Medicine · 2020
    Trial
  3. Trial
  4. Vitamin A Uses Its Superpowers to Combat Vascular Malformations.JACC. Basic to translational science · 2026
    Article
  5. Article
  6. Review
  7. Ruptured cerebral arteriovenous malformation associated with enlarged parietal foramina: a rare surgical case with pathogenetic implications.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2026
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Treatment of Brain Arteriovenous Malformations.Advances and technical standards in neurosurgery · 2024
    Article
  18. Review
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 6 institutions in 1 country.

Nikolaos MouchtourisDivision of Neurovascular Surgery and Endovascular Neurosurgery, Department of Neurological Surgery, Thomas Jefferson University and Jefferson Hospital for Neuroscience, Philadelphia, Pennsylvania, USA.
Pascal M JabbourDivision of Neurovascular Surgery and Endovascular Neurosurgery, Department of Neurological Surgery, Thomas Jefferson University and Jefferson Hospital for Neuroscience, Philadelphia, Pennsylvania, USA.
Robert M StarkeDepartment of Neurological Surgery, University of Virginia School of Medicine, Charlottesville, Virginia, USA.
David M HasanDepartment of Neurosurgery, University of Iowa, Iowa City, Iowa, USA.
Mario Zanaty1] Division of Neurovascular Surgery and Endovascular Neurosurgery, Department of Neurological Surgery, Thomas Jefferson University and Jefferson Hospital for Neuroscience, Philadelphia, Pennsylvania, USA [2] Department of Neurosurgery, University of Iowa, Iowa City, Iowa, USA.
Thana TheofanisDivision of Neurovascular Surgery and Endovascular Neurosurgery, Department of Neurological Surgery, Thomas Jefferson University and Jefferson Hospital for Neuroscience, Philadelphia, Pennsylvania, USA.
Dale DingDepartment of Neurological Surgery, University of Virginia School of Medicine, Charlottesville, Virginia, USA.
Stavropoula I TjoumakarisDivision of Neurovascular Surgery and Endovascular Neurosurgery, Department of Neurological Surgery, Thomas Jefferson University and Jefferson Hospital for Neuroscience, Philadelphia, Pennsylvania, USA.
Aaron S DumontDepartment of Neurological Surgery, Tulane University School of Medicine, New Orleans, Louisiana, USA.
George M GhobrialDivision of Neurovascular Surgery and Endovascular Neurosurgery, Department of Neurological Surgery, Thomas Jefferson University and Jefferson Hospital for Neuroscience, Philadelphia, Pennsylvania, USA.
David KungDivision of Neurovascular Surgery and Endovascular Neurosurgery, Department of Neurological Surgery, Thomas Jefferson University and Jefferson Hospital for Neuroscience, Philadelphia, Pennsylvania, USA.
Robert H RosenwasserDivision of Neurovascular Surgery and Endovascular Neurosurgery, Department of Neurological Surgery, Thomas Jefferson University and Jefferson Hospital for Neuroscience, Philadelphia, Pennsylvania, USA.
Nohra ChalouhiDivision of Neurovascular Surgery and Endovascular Neurosurgery, Department of Neurological Surgery, Thomas Jefferson University and Jefferson Hospital for Neuroscience, Philadelphia, Pennsylvania, USA.
Jefferson Hospital for Neuroscience · USNeurological Surgery · USThomas Jefferson University · USUniversity of Virginia · USTulane University · USUniversity of Iowa · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

AnimalsCell Adhesion MoleculesEndothelial CellsHumansInflammationIntracranial Arteriovenous MalformationsLeukocytesMatrix Metalloproteinase 9Polymorphism, Single NucleotideReceptors, NotchSignal TransductionUp-RegulationCell Adhesion MoleculesMatrix Metalloproteinase 9MMP9 protein, humanReceptors, Notch

Identifiers

PMID25407267
PMCPMC4426734
OpenAlexW1963992862

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.