Evidence map›Paper›PMID 29633884›Full record

ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2018

Gelatinolytic activity of autocrine matrix metalloproteinase-9 leads to endothelial de-arrangement in Moyamoya disease.

Kinga G Blecharz-Lang, Vincent Prinz, Małgorzata Burek, Dietmar Frey, Tobias Schenkel, Susanne M Krug, Michael Fromm, Peter Vajkoczy

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

25 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Moyamoya Disease: Pathophysiology, Diagnosis, and Treatment.Deutsches Arzteblatt international · 2025
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Molecular Biomarkers Affecting Moyamoya Disease.Advances and technical standards in neurosurgery · 2024
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. The Genetic Basis of Moyamoya Disease.Translational stroke research · 2022
    Review
  18. Observational
  19. Mutations ofJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
    Article
  20. Pathological Circulating Factors in Moyamoya Disease.International journal of molecular sciences · 2021
    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

8 authors at 2 institutions in 1 country.

Kinga G Blecharz-Lang1 Department of Experimental Neurosurgery, Charité - Universitätsmedizin Berlin, Berlin, Germany.
Vincent Prinz2 Department of Neurosurgery, Charité - Universitätsmedizin Berlin, Berlin, Germany.
Małgorzata Burek3 Department of Anaesthesia and Critical Care, University of Würzburg, Würzburg, Germany.
Dietmar Frey2 Department of Neurosurgery, Charité - Universitätsmedizin Berlin, Berlin, Germany.
Tobias Schenkel1 Department of Experimental Neurosurgery, Charité - Universitätsmedizin Berlin, Berlin, Germany.
Susanne M Krug4 Institute of Clinical Physiology, Charité - Universitätsmedizin Berlin, Berlin, Germany.
Michael Fromm4 Institute of Clinical Physiology, Charité - Universitätsmedizin Berlin, Berlin, Germany.
Peter Vajkoczy1 Department of Experimental Neurosurgery, Charité - Universitätsmedizin Berlin, Berlin, Germany.
Charité - Universitätsmedizin Berlin · DEUniversity of Würzburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Moyamoya disease (MMD) is a rare steno-occlusive cerebrovascular disorder. Mechanisms driving the formation of aberrant MMD vessels remain elusive. We collected serum and vessel specimens from MMD and atherosclerotic cerebrovascular disease (ACVD) patients serving as controls due to the same hypoxic stimulus but substantial differences in terms of vascular features. Based on patient material and an in vitro model mimicking ACVD and MMD conditions, matrix metalloproteinase-9 (MMP-9) and vascular-endothelial growth factor (VEGF) were tested for their potential involvement in cerebrovascular disintegration. While serum concentration of both molecules did not significantly differ in both patient groups, excessive collagenase activity and lowered collagen IV protein amount in MMD vessels pointed to a focal MMP-9 activity at the affected vessel sites. We observed overexpressed and autocrinely secreted MMP-9 and VEGF along with disturbances of EC-matrix interactions in MMD but not ACVD serum-treated cEND cells. These seemingly brain-specific effects were partially attenuated by VEGF signaling inhibition suggesting its role in the MMD etiology. In conclusion, our findings support the understanding of the high incidence of hemorrhagic and ischemic events in MMD and provide the basis for novel therapeutic strategies stopping or slowing the development of fragile cerebrovasculature or micro-bleeds characterizing the disease.

Indexed as

Endothelial CellsEndothelium, VascularHumansIn Vitro TechniquesMatrix Metalloproteinase 9Moyamoya DiseaseVascular Endothelial Growth Factor AMatrix Metalloproteinase 9Vascular Endothelial Growth Factor AVEGFA protein, humanangiogenesiscytokineendothelial cellMoyamoya diseasetight junction

Identifiers

PMID29633884
PMCPMC6259317
OpenAlexW2798083223

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.