Evidence map›Paper›PMID 35411318›Full record

ArticleJACC. Basic to translational science2022

Hyperadhesive von Willebrand Factor Promotes Extracellular Vesicle-Induced Angiogenesis: Implication for LVAD-Induced Bleeding.

Mengchen Yang, Katie L Houck, Xinlong Dong, Maria Hernandez, Yi Wang, Sriram S Nathan, Xiaoping Wu, Vahid Afshar-Kharghan, Xiaoyun Fu, Miguel A Cruz and 3 more

Open access · goldAbstract read
In one paragraph

Article in JACC. Basic to translational science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 2 pooled it
1.8field-weighted citation impact, top 16% 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

14 citing papers in PubMed, 2 syntheses or guidelines pooled it, 24 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Hyperadhesive von Willebrand Factor Contributes to Pathogenesis of Preeclampsia.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Article
  4. Review
  5. Article
  6. Observational
  7. Observational
  8. Review
  9. Review
  10. Article
  11. Von Willebrand factor and the thrombophilia of severe COVID-19:Research and practice in thrombosis and haemostasis · 2023
    Article
  12. Review
  13. Article
  14. Article
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 2 countries.

Mengchen YangBloodworks Research Institute, Seattle, Washington, USA.
Katie L HouckBloodworks Research Institute, Seattle, Washington, USA.
Xinlong DongBloodworks Research Institute, Seattle, Washington, USA.
Maria HernandezCenter for Advanced Heart Failure, University of Texas at Houston, Houston, Texas, USA.
Yi WangBloodworks Research Institute, Seattle, Washington, USA.
Sriram S NathanCenter for Advanced Heart Failure, University of Texas at Houston, Houston, Texas, USA.
Xiaoping WuDepartment of Pathology, University of Washington School of Medicine, Seattle, Washington, USA.
Vahid Afshar-KharghanDivision of Internal Medicine, Department of Pulmonary Medicine, MD Anderson Cancer Center, University of Texas, Houston, Texas, USA.
Xiaoyun FuBloodworks Research Institute, Seattle, Washington, USA.
Miguel A CruzCardiovascular Research Section, Department of Medicine, Baylor College of Medicine.
Jianning ZhangDepartment of Neurosurgery, Tianjin Medical University General Hospital, Tianjin, China.
Angelo NascimbeneCenter for Advanced Heart Failure, University of Texas at Houston, Houston, Texas, USA.
Jing-Fei DongBloodworks Research Institute, Seattle, Washington, USA.
Bloodworks Northwest · USThe University of Texas Health Science Center at Houston · USUniversity of Washington · USBaylor College of Medicine · USThe University of Texas MD Anderson Cancer Center · USTianjin Medical University General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bleeding associated with left ventricular assist device (LVAD) implantation has been attributed to the loss of large von Willebrand factor (VWF) multimers to excessive cleavage by ADAMTS-13, but this mechanism is not fully supported by the current evidence. We analyzed VWF reactivity in longitudinal samples from LVAD patients and studied normal VWF and platelets exposed to high shear stress to show that VWF became hyperadhesive in LVAD patients to induce platelet microvesiculation. Platelet microvesicles activated endothelial cells, induced vascular permeability, and promoted angiogenesis in a VWF-dependent manner. Our findings suggest that LVAD-driven high shear stress primarily activates VWF, rather than inducing cleavage in the majority of patients.

Indexed as

ADAMTS-13:Ag, ADAMTS-13 antigenangiogenesisAVS, aortic vascular segmentaVWS, acquired von Willebrand syndromeEC, endothelial cellEV, extracellular vesicleEVFP, extracellular vesicle–free plasmaextracellular vesiclesGI, gastrointestinalGOF, gain of functionGP, glycoproteinGPM, growth factor-poor mediumGRM, growth factor-rich mediumHSS, high shear stressleft ventricular assist devicesLVAD, left ventricular assist devicepEV, extracellular vesicle from von Willebrand factor-activated plateletsplateletsPS, phosphatidylserineshear stressSIPA, shear-induced platelet aggregationULVWF, ultra-large von Willebrand factorVEGF, vascular endothelial growth factorvon Willebrand factorVWF:Ag, von Willebrand factor antigenVWF:CB, von Willebrand factor binding to collagenVWF:pp, von Willebrand factor propeptideVWF, von Willebrand factor

Identifiers

PMID35411318
PMCPMC8993768
OpenAlexW4223472372

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.