Evidence map›Paper›PMID 16772609›Full record

ArticleBlood2006

Activation-independent platelet adhesion and aggregation under elevated shear stress.

Zaverio M Ruggeri, Jennifer N Orje, Rolf Habermann, Augusto B Federici, Armin J Reininger

Open access · greenAbstract read
In one paragraph

Article in Blood, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 169 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
169citing papers in PubMed, 1 pooled it
7.4field-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.

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

169 citing papers in PubMed, 1 synthesis or guideline pooled it, 408 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Review
  7. Hemodynamic consequences of TEVAR with different configurations ofFrontiers in cardiovascular medicine · 2026
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  12. Review
  13. PA System in the Pathogenesis of Ischemic Stroke.Arteriosclerosis, thrombosis, and vascular biology · 2025
    Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Platelet Adhesion and Activation in an ECMO Thrombosis-on-a-Chip Model.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  20. Article

109 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

5 authors at 1 institution in 1 country.

Zaverio M RuggeriThe Scripps Research Institute-MEM 175, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA. ruggeri@scripps.edu
Jennifer N Orje
Rolf Habermann
Augusto B Federici
Armin J Reininger
Thrombosis Research Institute · GB

Funding

THROMBUS FORMATION IN BABOONSP01HL031950 · NHLBI · SCRIPPS RESEARCH INSTITUTE, THE · PI GRIFFIN, JOHN H · 1985 to 2015
$29.4M
STRUCTURE/FUNCTION OF PLATELET MEMBRANE GLYCOPROTEINSR37HL042846 · NHLBI · SCRIPPS RESEARCH INSTITUTE, THE · PI RUGGERI, ZAVERIO M · 1999 to 2008
$4.1M
STRUCTURE &FUNCTION OF PLATELET MEMBRANE GLYCOPROTEINSR01HL042846 · NHLBI · SCRIPPS RESEARCH INSTITUTE, THE · PI RUGGERI, ZAVERIO M · 1989 to 2014
$2.4M
NHLBI NIH HHS HL 31950NHLBI NIH HHS HL 42846NHLBI NIH HHS HL 70818NHLBI NIH HHS HL 78728
6 · The paper itself

Abstract

Platelet aggregation, which contributes to bleeding arrest and also to thrombovascular disorders, is thought to initiate after signaling-induced activation. We found that this paradigm does not apply under blood flow conditions comparable to those existing in stenotic coronary arteries. Platelets interacting with immobilized von Willebrand factor (VWF) aggregate independently of activation when soluble VWF is present and the shear rate exceeds 10 000 s(-1) (shear stress = 400 dyn/cm(2)). Above this threshold, active A1 domains become exposed in soluble VWF multimers and can bind to glycoprotein Ibalpha, promoting additional platelet recruitment. Aggregates thus formed are unstable until the shear rate approaches 20 000 s(-1) (shear stress = 800 dyn/cm.(2)). Above this threshold, adherent platelets at the interface of surface-immobilized and membrane-bound VWF are stretched into elongated structures and become the core of aggregates that can persist on the surface for minutes. When isolated dimeric A1 domain is present instead of native VWF multimers, activation-independent platelet aggregation occurs without requiring shear stress above a threshold level, but aggregates never become firmly attached to the surface and progressively disaggregate as shear rate exceeds 6000 s(-1). Platelet and VWF modulation by hydrodynamic force is a mechanism for activation-independent aggregation that may support thrombotic arterial occlusion.

Indexed as

Blood PlateletsHemorheologyHumansIn Vitro TechniquesMembrane GlycoproteinsMembrane ProteinsMicroscopy, Electron, ScanningMultiprotein ComplexesPlatelet ActivationPlatelet AdhesivenessPlatelet AggregationPlatelet Glycoprotein GPIb-IX ComplexProtein BindingProtein Structure, TertiarySolubilityStress, Mechanicaladhesion receptorMembrane GlycoproteinsMembrane ProteinsMultiprotein ComplexesPlatelet Glycoprotein GPIb-IX Complexvon Willebrand Factor

Identifiers

PMID16772609
PMCPMC1895550
OpenAlexW2046417991

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.