Evidence map›Paper›PMID 29383704›Full record

ArticleBritish journal of haematology2018

Platelets at the crossroads of thrombosis, inflammation and haemolysis.

Sebastian Vogel, Swee Lay Thein

Open access · greenAbstract read
In one paragraph

Article in British journal of haematology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

22 citing papers in PubMed, 38 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Depolarized Mitochondrial Membrane Potential and Elevated Calcium in Platelets of Sickle Cell Disease.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2023
    Article
  8. Article
  9. Inflammasomes-New Contributors to Blood Diseases.International journal of molecular sciences · 2022
    Review
  10. Gegen Qinlian pills alleviate carrageenan-induced thrombosis in mice model by regulating the HMGB1/NF-κB/NLRP3 signaling.Phytomedicine : international journal of phytotherapy and phytopharmacology · 2022
    Article
  11. Article
  12. Article
  13. Linking Labile Heme with Thrombosis.Journal of clinical medicine · 2021
    Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. 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

2 authors at 1 institution in 1 country.

Sebastian VogelSickle Cell Branch, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, MD, USA.ORCID 0000-0002-3284-0464
Swee Lay TheinSickle Cell Branch, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
National Institutes of Health · US

Funding

Pathophysiology of Acute Pain in Patients with Sickle Cell DiseaseZIAHL006232 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI THEIN, SWEE LAY · 2017 to 2020
$6.4M
Intramural NIH HHS Z99 HL999999
6 · The paper itself

Abstract

Platelets play a critical role at the interphase of thrombosis and inflammation, key features in haemolysis-associated disorders. Exercising this role requires expression of pattern recognition receptors by platelets, including toll-like receptor 4 (TLR4) and nucleotide-binding domain leucine rich repeat containing protein 3 (NLRP3), the latter forming intraplatelet multiprotein inflammasome complexes. Platelets are a potential target of various damage-associated molecular pattern (DAMP) molecules, such as free haem, a degradation by-product of haemoglobin oxidation during haemolysis, and high-mobility group box 1 (HMGB1), a DNA-binding protein released by dying or stressed cells and activated platelets. We have recently identified platelet TLR4, NLRP3, and Bruton tyrosine kinase (BTK) as critical regulators of platelet aggregation and thrombus formation, suggesting that the BTK inhibitor ibrutinib is a potential therapeutic target. Increasing evidence suggests that these and other DAMP-driven signalling mechanisms employed by platelets might be key in mediating inflammation and thrombosis encountered in haemolytic disorders. However, the precise regulatory triggers and their clinical relevance are poorly understood. We provide new insights into these less-well characterised platelet mechanisms, which are potentially targetable in haemolytic disorders.

Indexed as

Anemia, Sickle CellBlood PlateletsHematologic DiseasesHemolysisHMGB1 ProteinHumansInflammationNLR Family, Pyrin Domain-Containing 3 ProteinSignal TransductionThrombosisHMGB1 ProteinHMGB1 protein, humanNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanhaemolysisinflammationplateletssickle cell diseasethrombosis

Identifiers

PMID29383704
PMCPMC6419732
OpenAlexW2791842742

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.