Evidence map›Paper›PMID 26474813›Full record

ArticleBlood2015

Necrotic platelets provide a procoagulant surface during thrombosis.

Vu Minh Hua, Latasha Abeynaike, Elias Glaros, Heather Campbell, Leonardo Pasalic, Philip J Hogg, Vivien M Y Chen

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

56 citing papers in PubMed, 108 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Platelets and Thrombotic Antiphospholipid Syndrome.Journal of clinical medicine · 2024
    Review
  13. Article
  14. Article
  15. Immunothrombosis in neurovascular disease.Research and practice in thrombosis and haemostasis · 2024
    Article
  16. Research and practice in thrombosis and haemostasis · 2024
    Article
  17. A thrombus is formed by a gradient of platelet activation and procoagulant endothelium.Research and practice in thrombosis and haemostasis · 2023
    Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 1 country.

Vu Minh HuaLowy Cancer Research Centre and Prince of Wales Clinical School, University of New South Wales, Sydney, New South Wales, Australia;
Latasha AbeynaikeLowy Cancer Research Centre and Prince of Wales Clinical School, University of New South Wales, Sydney, New South Wales, Australia;
Elias GlarosLowy Cancer Research Centre and Prince of Wales Clinical School, University of New South Wales, Sydney, New South Wales, Australia;
Heather CampbellLowy Cancer Research Centre and Prince of Wales Clinical School, University of New South Wales, Sydney, New South Wales, Australia;
Leonardo PasalicHaematology, Institute of Clinical Pathology and Medical Research, Westmead, New South Wales, Australia;
Philip J HoggThe Centenary Institute, Newtown, Sydney, New South Wales, Australia; National Health and Medical Research Council Clinical Trials Centre, University of Sydney, Sydney, New South Wales, Australia;ORCID http://orcid.org/0000-0001-6486-2863
Vivien M Y ChenLowy Cancer Research Centre and Prince of Wales Clinical School, University of New South Wales, Sydney, New South Wales, Australia; Haematology, Concord Repatriation and General Hospital, Sydney, New South Wales, Australia; and ANZAC Research Institute, Concord, New South Wales, Australia.
UNSW Sydney · AUConcord Repatriation General Hospital · AUThe University of Sydney · AUWestmead Institute for Medical Research · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A subpopulation of platelets fulfills a procoagulant role in hemostasis and thrombosis by enabling the thrombin burst required for fibrin formation and clot stability at the site of vascular injury. Excess procoagulant activity is linked with pathological thrombosis. The identity of the procoagulant platelet has been elusive. The cell death marker 4-[N-(S-glutathionylacetyl)amino]phenylarsonous acid (GSAO) rapidly enters a subpopulation of agonist-stimulated platelets via an organic anion-transporting polypeptide and is retained in the cytosol through covalent reaction with protein dithiols. Labeling with GSAO, together with exposure of P-selectin, distinguishes necrotic from apoptotic platelets and correlates with procoagulant potential. GSAO(+) platelets form in occluding murine thrombi after ferric chloride injury and are attenuated with megakaryocyte-directed deletion of the cyclophilin D gene. These platelets form a procoagulant surface, supporting fibrin formation, and reduction in GSAO(+) platelets is associated with reduction in platelet thrombus size and fibrin formation. Analysis of platelets from human subjects receiving aspirin therapy indicates that these procoagulant platelets form despite aspirin therapy, but are attenuated by inhibition of the necrosis pathway. These findings indicate that the major subpopulation of platelets involved in fibrin formation are formed via regulated necrosis involving cyclophilin D, and that they may be targeted independent of platelet activation.

Indexed as

AnimalsArsenicalsBiomarkersBlood PlateletsCells, CulturedCyclophilinsFlow CytometryGlutathioneHumansMiceMicroscopy, ConfocalNecrosisPeptidyl-Prolyl Isomerase DPlatelet ActivationThrombosis4-(N-(S-glutathionylacetyl)amino)phenylarsenoxideArsenicalsBiomarkersCyclophilinsGlutathionePeptidyl-Prolyl Isomerase DPPID protein, human

Identifiers

PMID26474813
PMCPMC4692145
OpenAlexW2344212065

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.