Evidence map›Paper›PMID 31119724›Full record

ArticleClinical and experimental immunology2019

Enhanced monocyte recruitment and delayed alternative macrophage polarization accompanies impaired repair following myocardial infarction in C57BL/6 compared to BALB/c mice.

I S Toor, D Rückerl, I Mair, A Thomson, A G Rossi, D E Newby, J E Allen, G A Gray

Open access · hybridAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

10 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Quo Vadis? Immunodynamics of Myeloid Cells after Myocardial Infarction.International journal of molecular sciences · 2022
    Review
  6. Article
  7. Review
  8. Monocyte recruitment and fate specification after myocardial infarction.American journal of physiology. Cell physiology · 2020
    Review
  9. Article
  10. 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

8 authors at 3 institutions in 1 country.

I S ToorBHF/University Centre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.ORCID 0000-0003-1564-491X
D RückerlFaculty of Biology, Medicine and Health, School of Biological Sciences, University of Manchester, Edinburgh, UK.ORCID 0000-0002-0206-1451
I MairMRC Centre for Inflammation Research, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.ORCID 0000-0002-7326-3114
A ThomsonBHF/University Centre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.
A G RossiMRC Centre for Inflammation Research, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.
D E NewbyBHF/University Centre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.
J E AllenFaculty of Biology, Medicine and Health, School of Biological Sciences, University of Manchester, Edinburgh, UK.ORCID 0000-0002-3829-066X
G A GrayBHF/University Centre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.ORCID 0000-0003-3104-3305
The Queen's Medical Research Institute · GBQueen's Medical Centre · GBUniversity of Manchester · GB

Funding

British Heart Foundation CH/09/002British Heart Foundation RE/13/3/30183British Heart Foundation RG/16/10/32375British Heart Foundation RM/13/2/30158Medical Research Council MR/K01207X/1Medical Research Council MR/K01207X/2Medical Research Council MR/K013386/1Wellcome Trust 104799/Z/14/ZWellcome Trust WT103782AIA
6 · The paper itself

Abstract

Activation of the innate immune response following myocardial infarction (MI) is essential for infarct repair. Preclinical models of MI commonly use C57BL/6 mice, which have a type 1-dominant immune response, whereas other mouse strains such as BALB/c mice have a type 2-dominant immune response. We compared C57BL/6 and BALB/c mice to investigate whether predisposition towards a proinflammatory phenotype influences the dynamics of the innate immune response to MI and associated infarct healing and the risk of cardiac rupture. MI was induced by permanent coronary artery ligation in 12-15-week-old male wild-type BALB/c and C57BL/6 mice. Prior to MI, C57BL/6 mice had a lower proportion of CD206

Indexed as

AnimalsCoronary VesselsGenotypeInflammationMacrophage ActivationMacrophagesMaleMiceMice, Inbred BALB CMice, Inbred C57BLMonocytesMyeloid CellsMyocardial InfarctionMyocardiumPhenotypeWound HealingBALB/cC57BL/6macrophage polarizationmonocytemyocardial infarction

Identifiers

PMID31119724
PMCPMC6718279
OpenAlexW2945617112

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.