Evidence map›Paper›PMID 23733341›Full record

ArticleBlood2013

A vasculo-protective circuit centered on lipoxin A4 and aspirin-triggered 15-epi-lipoxin A4 operative in murine microcirculation.

Vincenzo Brancaleone, Thomas Gobbetti, Nicolas Cenac, Pauline le Faouder, Bartomeu Colom, Roderick J Flower, Nathalie Vergnolle, Sussan Nourshargh, Mauro Perretti

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
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

54 citing papers in PubMed, 95 citations in OpenAlex.

  1. Trial
  2. Trial
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  4. Cell-cell interactions and bronchoconstrictor eicosanoid reduction with inhaled carbon monoxide and resolvin D1.American journal of physiology. Lung cellular and molecular physiology · 2014
    Trial
  5. FPR2 Agonism Attenuates Restenosis by Mitigating Neointimal Hyperplasia via ELOVL6.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  6. Article
  7. Review
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  10. Article
  11. Interferon-β regulates proresolving lipids to promote the resolution of acute airway inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. 15-Epi-LXAProceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  19. Review
  20. The dual role of platelet-innate immune cell interactions in thrombo-inflammation.Research and practice in thrombosis and haemostasis · 2020
    Review
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

9 authors at 3 institutions in 2 countries.

Vincenzo BrancaleoneWilliam Harvey Research Institute, Barts and The London School of Medicine, Queen Mary University of London, London, United Kingdom.
Thomas Gobbetti
Nicolas Cenac
Pauline le Faouder
Bartomeu Colom
Roderick J Flower
Nathalie Vergnolle
Sussan Nourshargh
Mauro Perretti
William Harvey Research Institute · GBUniversité Toulouse III - Paul Sabatier · FRQueen Mary University of London · GB

Funding

Wellcome Trust 086867/Z/08/Z
6 · The paper itself

Abstract

Endogenous protective pathways mitigate the overshooting of inflammation after sterile or infectious injury. Here we report that formyl peptide receptor 2 (Fpr2/3) null mice display a major phenotype with exacerbated vascular inflammation observed postischemia reperfusion (IR) injury of the mesenteric artery, characterized by marked neutrophil adhesion and extravasation as visualized by intravital microscopy. Analysis of endogenous agonists for Fpr2/3 revealed that lipoxin A4 (LXA4) was generated by platelet/neutrophil aggregates during ischemia: this cellular response was attenuated in Fpr2/3(-/-) mice; hence, LXA4 levels were lower after 30 minutes' ischemia, and associated with augmented vascular inflammation in the reperfusion (45-180 minutes) phase. Exogenous delivery of LXA4 attenuated IR-mediated inflammation in Fpr2/3(+/+) but not Fpr2/3(-/-) mice; conversely, an Fpr2/3 antagonist skewed the vascular phenotype of Fpr2/3(+/+) mice to that of Fpr2/3(-/-) animals. Such LXA4-based circuit could be activated by aspirin (30-100 mg/kg), which triggered formation of 15-epi-LXA4 in wild-type mice, yet it was effective in Fpr2/3(-/-) mice. In summary, we propose that during ischemia, neutrophil Fpr2/3 controls platelet/neutrophil aggregates with the rapid generation of circulating LXA4, which in turn modulates downstream vascular inflammatory responses evident during the reperfusion phase.

Indexed as

Blood VesselsCytoprotectionAnimalsAnti-Inflammatory AgentsAspirinLipoxinsMaleMiceMice, KnockoutMicrocirculationModels, BiologicalProdrugsReceptors, Formyl PeptideReperfusion InjurySignal TransductionAnti-Inflammatory AgentsAspirinformyl peptide receptor 2, mouselipoxin A4LipoxinsProdrugsReceptors, Formyl Peptide

Identifiers

PMID23733341
PMCPMC3724196
OpenAlexW1974048267

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.