Evidence map›Paper›PMID 21048155›Full record

ArticleBlood2011

Endothelial von Willebrand factor regulates angiogenesis.

Richard D Starke, Francesco Ferraro, Koralia E Paschalaki, Nicola H Dryden, Thomas A J McKinnon, Rachel E Sutton, Elspeth M Payne, Dorian O Haskard, Alun D Hughes, Daniel F Cutler and 2 more

Registry-linked trialOpen access · greenAbstract read
In one paragraph

Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02460458 (Type 3 Von Willebrand International Registries Inhibitor Prospective Study), which is not on this map. Cited by 225 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
225citing papers in PubMed, 3 pooled it
7.8field-weighted citation impact, top 2% 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.

NCT02460458 completednot on this mapstarted 2012, after this paper: background citation

Type 3 Von Willebrand International Registries Inhibitor Prospective Study

TypeobservationalSponsorFondazione Angelo Bianchi BonomiRan2012 to 2023Enrolled265ConditionsType 3 Von Willebrand's DiseaseArmsVon Willebrand Factor
3 · Its place in the literature

Who cites it

225 citing papers in PubMed, 3 syntheses or guidelines pooled it, 491 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Guideline
  4. Trial
  5. Trial
  6. Trial
  7. Trial
  8. Inherited human group IVA cytosolic phospholipase A2 deficiency abolishes platelet, endothelial, and leucocyte eicosanoid generation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015
    Trial
  9. Review
  10. Article
  11. von Willebrand disease: an illustrated review.Research and practice in thrombosis and haemostasis · 2026
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review

165 more citing papers are in PubMed but not listed here.

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

12 authors at 3 institutions in 1 country.

Richard D StarkeCardiovascular Sciences, National Heart and Lung Institute, Faculty of Medicine, Hammersmith Campus, Imperial College Academic Health Sciences Centre, Imperial College London, London, UK.
Francesco Ferraro
Koralia E Paschalaki
Nicola H Dryden
Thomas A J McKinnon
Rachel E Sutton
Elspeth M Payne
Dorian O Haskard
Alun D Hughes
Daniel F Cutler
Mike A Laffan
Anna M Randi
Imperial College London · GBMRC Laboratory for Molecular Cell Biology · GBImperial College Healthcare NHS Trust · GB

Funding

British Heart Foundation FS/10/047/28393British Heart Foundation FS/10/47/28393Medical Research Council G0600868Medical Research Council MC_U122665003Wellcome Trust
6 · The paper itself

Abstract

The regulation of blood vessel formation is of fundamental importance to many physiological processes, and angiogenesis is a major area for novel therapeutic approaches to diseases from ischemia to cancer. A poorly understood clinical manifestation of pathological angiogenesis is angiodysplasia, vascular malformations that cause severe gastrointestinal bleeding. Angiodysplasia can be associated with von Willebrand disease (VWD), the most common bleeding disorder in man. VWD is caused by a defect or deficiency in von Willebrand factor (VWF), a glycoprotein essential for normal hemostasis that is involved in inflammation. We hypothesized that VWF regulates angiogenesis. Inhibition of VWF expression by short interfering RNA (siRNA) in endothelial cells (ECs) caused increased in vitro angiogenesis and increased vascular endothelial growth factor (VEGF) receptor-2 (VEGFR-2)-dependent proliferation and migration, coupled to decreased integrin αvβ3 levels and increased angiopoietin (Ang)-2 release. ECs expanded from blood-derived endothelial progenitor cells of VWD patients confirmed these results. Finally, 2 different approaches, in situ and in vivo, showed increased vascularization in VWF-deficient mice. We therefore identify a new function of VWF in ECs, which confirms VWF as a protein with multiple vascular roles and defines a novel link between hemostasis and angiogenesis. These results may have important consequences for the management of VWD, with potential therapeutic implications for vascular diseases.

Indexed as

Neovascularization, PhysiologicAdultAged, 80 and overAngiopoietin-2AnimalsCell LineCell MovementCell ProliferationEndothelial CellsFemaleHemostasisHumansImmunoblottingIntegrin alphaVbeta3MaleMiceAngiopoietin-2Integrin alphaVbeta3Vascular Endothelial Growth Factor Receptor-2von Willebrand Factor

Identifiers

PMID21048155
PMCPMC3035068
OpenAlexW2066589515

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.