Evidence map›Paper›PMID 32478907›Full record

ArticleTransfusion2020

Von Willebrand factor as a thrombotic and inflammatory mediator in critical illness.

William E Plautz, Zachary A Matthay, Marian A Rollins-Raval, Jay S Raval, Lucy Z Kornblith, Matthew D Neal

Open access · greenAbstract read
In one paragraph

Article in Transfusion, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

17 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Biological attributes of zinc-dependent endopeptidases in endothelial dysfunction associated with sepsis: a narrative review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Observational
  16. Trauma-induced coagulopathy.Nature reviews. Disease primers · 2021
    Review
  17. 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

6 authors at 3 institutions in 1 country.

William E PlautzDepartment of Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania.ORCID 0000-0002-9140-1023
Zachary A MatthayDepartment of Surgery, University of California, San Francisco, San Francisco, California.
Marian A Rollins-RavalDepartment of Pathology, University of New Mexico, Albuquerque, New Mexico.
Jay S RavalDepartment of Pathology, University of New Mexico, Albuquerque, New Mexico.
Lucy Z KornblithDepartment of Surgery, University of California, San Francisco, San Francisco, California.
Matthew D NealDepartment of Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania.
San Francisco General Hospital · USUniversity of New Mexico · USUniversity of Pittsburgh Medical Center · US

Funding

Post-Injury Platelet Biology: Mechanisms and OutcomesK23GM130892 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KORNBLITH, LUCY ZUMWINKLE · 2018 to 2022
$995k
NIGMS NIH HHS K23 GM130892
6 · The paper itself

Abstract

The endothelial exocytosis of high-molecular-weight multimeric von Willebrand factor (vWF) may occur in critical illness states, including trauma and sepsis, leading to the sustained elevation and altered composition of plasma vWF. These critical illnesses involve the common process of sympathoadrenal activation and loss of the endothelial glycocalyx. As a prothrombotic and proinflammatory molecule that interacts with the endothelium, the alterations exhibited by vWF in critical illness have been implicated in the development and damaging effects of downstream pathologies, such as disseminated intravascular coagulation and systemic inflammatory response syndrome. Given the role of vWF in these pathologies, there has been a recent push to further understand how the molecule may be involved in the pathophysiology of related diseases, such as trauma-induced coagulopathy and acute renal injury, which are also known to develop secondarily to critical illness states. Elucidation of the role of vWF across the broader spectrum of generalized pathologies may provide a basis for the development of novel preventative and restorative measures, while also bolstering the scaffold of more widely used treatments, such as the administration of plasma-containing blood products.

Indexed as

Critical IllnessAcute Kidney InjuryADAMTS13 ProteinBlood CoagulationBlood Coagulation DisordersEndothelium, VascularHumansInflammation MediatorsSepsisvon Willebrand FactorWounds and InjuriesADAMTS13 ProteinInflammation Mediatorsvon Willebrand Factor

Identifiers

PMID32478907
PMCPMC9053104
OpenAlexW3029682581

What OpenQuestion holds

Textmetadata
LicenceTDM
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.