Evidence map›Paper›PMID 25982896›Full record

ArticleEuropean heart journal2015

Acute myocardial infarction activates distinct inflammation and proliferation pathways in circulating monocytes, prior to recruitment, and identified through conserved transcriptional responses in mice and humans.

Neil Ruparelia, Jernej Godec, Regent Lee, Joshua T Chai, Erica Dall'Armellina, Debra McAndrew, Janet E Digby, J Colin Forfar, Bernard D Prendergast, Rajesh K Kharbanda and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in European heart journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 2 pooled it
6.4field-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

69 citing papers in PubMed, 2 syntheses or guidelines pooled it, 121 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
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  7. Article
  8. The spleen in ischaemic heart disease.Nature reviews. Cardiology · 2025
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  15. Review
  16. Immunometabolism in atherosclerotic disorders.Nature cardiovascular research · 2024
    Review
  17. Review
  18. Infliximab Limits Injury in Myocardial Infarction.Journal of the American Heart Association · 2024
    Article
  19. Article
  20. Review

9 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

16 authors at 3 institutions in 2 countries.

Neil RupareliaDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, John Radcliffe Hospital, University of Oxford, Headley Way, Oxford OX3 9DU, UK Oxford Heart Centre, John Radcliffe Hospital, Headley Way, Oxford OX3 9DU, UK.
Jernej GodecDana-Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA.
Regent LeeDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, John Radcliffe Hospital, University of Oxford, Headley Way, Oxford OX3 9DU, UK.
Joshua T ChaiDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, John Radcliffe Hospital, University of Oxford, Headley Way, Oxford OX3 9DU, UK.
Erica Dall'ArmellinaDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, John Radcliffe Hospital, University of Oxford, Headley Way, Oxford OX3 9DU, UK Acute Vascular Imaging Centre, Radcliffe Department of Medicine, John Radcliffe Hospital, University of Oxford, Headley Way, Oxford OX3 9DU, UK.
Debra McAndrewDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, John Radcliffe Hospital, University of Oxford, Headley Way, Oxford OX3 9DU, UK.
Janet E DigbyDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, John Radcliffe Hospital, University of Oxford, Headley Way, Oxford OX3 9DU, UK.
J Colin ForfarOxford Heart Centre, John Radcliffe Hospital, Headley Way, Oxford OX3 9DU, UK.
Bernard D PrendergastOxford Heart Centre, John Radcliffe Hospital, Headley Way, Oxford OX3 9DU, UK.
Rajesh K KharbandaOxford Heart Centre, John Radcliffe Hospital, Headley Way, Oxford OX3 9DU, UK.
Adrian P BanningOxford Heart Centre, John Radcliffe Hospital, Headley Way, Oxford OX3 9DU, UK.
Stefan NeubauerDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, John Radcliffe Hospital, University of Oxford, Headley Way, Oxford OX3 9DU, UK.
Craig A LygateDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, John Radcliffe Hospital, University of Oxford, Headley Way, Oxford OX3 9DU, UK.
Keith M ChannonDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, John Radcliffe Hospital, University of Oxford, Headley Way, Oxford OX3 9DU, UK Oxford Heart Centre, John Radcliffe Hospital, Headley Way, Oxford OX3 9DU, UK.
Nicholas W HainingDana-Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA.
Robin P ChoudhuryDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, John Radcliffe Hospital, University of Oxford, Headley Way, Oxford OX3 9DU, UK Oxford Heart Centre, John Radcliffe Hospital, Headley Way, Oxford OX3 9DU, UK Acute Vascular Imaging Centre, Radcliffe Department of Medicine, John Radcliffe Hospital, University of Oxford, Headley Way, Oxford OX3 9DU, UK robin.choudhury@cardiov.ox.ac.uk.
John Radcliffe Hospital · GBUniversity of Oxford · GBDana-Farber Cancer Institute · US

Funding

British Heart Foundation FS/13/71/30378British Heart Foundation PG/12/46/29673British Heart Foundation RG/13/8/30266Medical Research Council G0900747Medical Research Council MR/K00266X/1Wellcome Trust 088291Wellcome Trust 090532
6 · The paper itself

Abstract

aimsMonocytes play critical roles in tissue injury and repair following acute myocardial infarction (AMI). Specifically targeting inflammatory monocytes in experimental models leads to reduced infarct size and improved healing. However, data from humans are sparse, and it remains unclear whether monocytes play an equally important role in humans. The aim of this study was to investigate whether the monocyte response following AMI is conserved between humans and mice and interrogate patterns of gene expression to identify regulated functions. METHODS AND

resultsThirty patients (AMI) and 24 control patients (stable coronary atherosclerosis) were enrolled. Female C57BL/6J mice (n = 6/group) underwent AMI by surgical coronary ligation. Myocardial injury was quantified by magnetic resonance imaging (human) and echocardiography (mice). Peripheral monocytes were isolated at presentation and at 48 h. RNA from separated monocytes was hybridized to Illumina beadchips. Acute myocardial infarction resulted in a significant peripheral monocytosis in both species that positively correlated with the extent of myocardial injury. Analysis of the monocyte transcriptome following AMI demonstrated significant conservation and identified inflammation and mitosis as central processes to this response. These findings were validated in both species.

conclusionsOur findings show that the monocyte transcriptome is conserved between mice and humans following AMI. Patterns of gene expression associated with inflammation and proliferation appear to be switched on prior to their infiltration of injured myocardium suggesting that the specific targeting of inflammatory and proliferative processes in these immune cells in humans are possible therapeutic strategies. Importantly, they could be effective in the hours after AMI.

Indexed as

AgedAnimalsCase-Control StudiesCell ProliferationFemaleGene Expression ProfilingHumansInflammationLeukocytes, MononuclearLigationMagnetic Resonance AngiographyMaleMice, Inbred C57BLMiddle AgedMyocardial InfarctionPhenotypeAcute myocardial infarctionGenomicsInflammationMitosisMonocytes

Identifiers

PMID25982896
PMCPMC4571177
OpenAlexW2116912129

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Registered trials

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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.