Evidence map›Paper›PMID 23087356›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2012

Blood clots are rapidly assembled hemodynamic sensors: flow arrest triggers intraluminal thrombus contraction.

Ryan W Muthard, Scott L Diamond

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

74 citing papers in PubMed, 102 citations in OpenAlex.

  1. Article
  2. Review
  3. Rupture mechanics of blood clot fibrin fibers: A coarse-grained model study.Journal of the mechanics and physics of solids · 2025
    Article
  4. Article
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  6. Review
  7. Article
  8. Article
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  11. Article
  12. Recent Advances in Blood Cell-Inspired and Clot Targeted Thrombolytic Therapies.Journal of tissue engineering and regenerative medicine · 2023
    Review
  13. Blood clot contraction: Mechanisms, pathophysiology, and disease.Research and practice in thrombosis and haemostasis · 2023
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Thrombosis and Hemodynamics: external and intrathrombus gradients.Current opinion in biomedical engineering · 2021
    Article
  20. Review

14 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

2 authors at 1 institution in 1 country.

Ryan W MuthardDepartment of Chemical and Biomolecular Engineering, Vagelos Research Laboratory, Institute for Medicine and Engineering, University of Pennsylvania, Philadelphia, PA 19104, USA.
Scott L Diamond
University of Pennsylvania · US

Funding

Blood Systems BiologyR01HL103419 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI DIAMOND, SCOTT L · 2010 to 2019
$7.4M
NHLBI NIH HHS NIH R01HL103419NHLBI NIH HHS R01 HL103419
6 · The paper itself

Abstract

objectiveBlood clots form under flow during intravascular thrombosis or vessel leakage. Prevailing hemodynamics influence thrombus structure and may regulate contraction processes. A microfluidic device capable of flowing human blood over a side channel plugged with collagen (± tissue factor) was used to measure thrombus permeability (κ) and contraction at controlled transthrombus pressure drops. METHODS AND

resultsThe collagen (κ(collagen)=1.98 × 10(-11) cm(2)) supported formation of a 20-µm thick platelet layer, which unexpectedly underwent massive platelet retraction on flow arrest. This contraction resulted in a 5.34-fold increase in permeability because of collagen restructuring. Without stopping flow, platelet deposits (no fibrin) had a permeability of κ(platelet)=5.45 × 10(-14) cm(2) and platelet-fibrin thrombi had κ(thrombus)=2.71 × 10(-14) cm(2) for ΔP=20.7 to 23.4 mm Hg, the first ever measurements for clots formed under arterial flow (1130 s(-1) wall shear rate). Platelet sensing of flow cessation triggered a 4.6- to 6.5-fold (n=3, P<0.05) increase in contraction rate, which was also observed in a rigid, impermeable parallel-plate microfluidic device. This triggered contraction was blocked by the myosin IIA inhibitor blebbistatin and by inhibitors of thromboxane A2 (TXA(2)) and ADP signaling. In addition, flow arrest triggered platelet intracellular calcium mobilization, which was blocked by TXA(2)/ADP inhibitors. As clots become occlusive or blood pools following vessel leakage, the flow diminishes, consequently allowing full platelet retraction.

conclusionsFlow dilution of ADP and thromboxane regulates platelet contractility with prevailing hemodynamics, a newly defined flow-sensing mechanism to regulate clot function.

Indexed as

Cardiovascular Physiological PhenomenaAdenosine DiphosphateBlood CoagulationBlood PlateletsCalciumCollagenEquipment DesignHemodynamicsHeterocyclic Compounds, 4 or More RingsHumansIn Vitro TechniquesMicrofluidic Analytical TechniquesNonmuscle Myosin Type IIARegional Blood FlowSignal TransductionThrombosisAdenosine DiphosphateblebbistatinCalciumCollagenHeterocyclic Compounds, 4 or More RingsNonmuscle Myosin Type IIAThromboxane A2

Identifiers

PMID23087356
PMCPMC3586804
OpenAlexW2101613467

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.