Evidence map›Paper›PMID 30413433›Full record

ArticleBlood advances2018

The endogenous antimicrobial cathelicidin LL37 induces platelet activation and augments thrombus formation.

Maryam F Salamah, Divyashree Ravishankar, Xenia Kodji, Leonardo A Moraes, Harry F Williams, Thomas M Vallance, Dina A Albadawi, Rajendran Vaiyapuri, Kim Watson, Jonathan M Gibbins and 3 more

Open access · goldAbstract read
In one paragraph

Article in Blood advances, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
3.5field-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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.

  1. Pooled it
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  7. Article
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  14. LL-37 Triggers Antimicrobial Activity in Human Platelets.International journal of molecular sciences · 2023
    Article
  15. Article
  16. Article
  17. Review
  18. NET-(works) in arterial and venous thrombo-occlusive diseases.Frontiers in cardiovascular medicine · 2023
    Review
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  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

13 authors at 4 institutions in 2 countries.

Maryam F SalamahSchool of Pharmacy, University of Reading, Reading, United Kingdom.
Divyashree RavishankarSchool of Pharmacy, University of Reading, Reading, United Kingdom.
Xenia KodjiSection of Vascular Biology & Inflammation, School of Cardiovascular Medicine & Research, King's College London, London, United Kingdom.
Leonardo A MoraesDepartment of Physiology, National University of Singapore, Singapore.
Harry F WilliamsSchool of Pharmacy, University of Reading, Reading, United Kingdom.
Thomas M VallanceSchool of Pharmacy, University of Reading, Reading, United Kingdom.
Dina A AlbadawiSchool of Pharmacy, University of Reading, Reading, United Kingdom.
Rajendran VaiyapuriSchool of Pharmacy, University of Reading Malaysia, Johor, Malaysia.
Kim WatsonSchool of Biological Sciences, University of Reading, Reading, United Kingdom; and.
Jonathan M GibbinsSchool of Biological Sciences, University of Reading, Reading, United Kingdom; and.
Susan D BrainSection of Vascular Biology & Inflammation, School of Cardiovascular Medicine & Research, King's College London, London, United Kingdom.
Mauro PerrettiWilliam Harvey Research Institute, London, United Kingdom.
Sakthivel VaiyapuriSchool of Pharmacy, University of Reading, Reading, United Kingdom.ORCID 0000-0002-6006-6517
University of Reading · GBKing's College London · GBNational University of Singapore · SGWilliam Harvey Research Institute · GB

Funding

British Heart Foundation FS/16/65/32489British Heart Foundation PG/16/64/32311British Heart Foundation RG/09/011/28094Wellcome TrustWellcome Trust 204389/Z/16/Z
6 · The paper itself

Abstract

Platelet-associated complications including thrombosis, thrombocytopenia, and hemorrhage are commonly observed during various inflammatory diseases such as sepsis, inflammatory bowel disease, and psoriasis. Despite the reported evidence on numerous mechanisms/molecules that may contribute to the dysfunction of platelets, the primary mechanisms that underpin platelet-associated complications during inflammatory diseases are not fully established. Here, we report the discovery of formyl peptide receptor 2, FPR2/ALX, in platelets and its primary role in the development of platelet-associated complications via ligation with its ligand, LL37. LL37 acts as a powerful endogenous antimicrobial peptide, but it also regulates innate immune responses. We demonstrate the impact of LL37 in the modulation of platelet reactivity, hemostasis, and thrombosis. LL37 activates a range of platelet functions, enhances thrombus formation, and shortens the tail bleeding time in mice. By utilizing a pharmacological inhibitor and

Indexed as

Antimicrobial Cationic PeptidesBinding SitesBlood PlateletsCalciumCathelicidinsCyclic AMPHemostasisHumansPlatelet ActivationReceptors, Formyl PeptideReceptors, LipoxinSignal TransductionThrombosisAntimicrobial Cationic PeptidesCalciumCathelicidinsCyclic AMPFPR2 protein, humanReceptors, Formyl PeptideReceptors, Lipoxin

Identifiers

PMID30413433
PMCPMC6234361
OpenAlexW2900428167

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.