Evidence map›Paper›PMID 28302646›Full record

ArticleThe Journal of experimental medicine2017

Eosinophil-derived IL-4 drives progression of myocarditis to inflammatory dilated cardiomyopathy.

Nicola L Diny, G Christian Baldeviano, Monica V Talor, Jobert G Barin, SuFey Ong, Djahida Bedja, Allison G Hays, Nisha A Gilotra, Isabelle Coppens, Noel R Rose and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 2 pooled it
8.0field-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

62 citing papers in PubMed, 2 syntheses or guidelines pooled it, 100 citations in OpenAlex.

  1. Pooled it
  2. Myocardial Immune Cells: The Basis of Cardiac Immunology.Journal of immunology (Baltimore, Md. : 1950) · 2023
    Pooled it
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2 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

11 authors at 1 institution in 1 country.

Nicola L DinyW. Harry Feinstone Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD 21205.ORCID 0000-0002-9145-5216
G Christian BaldevianoDepartment of Pathology, School of Medicine, Johns Hopkins University, Baltimore, MD 21205.
Monica V TalorDepartment of Pathology, School of Medicine, Johns Hopkins University, Baltimore, MD 21205.
Jobert G BarinDepartment of Pathology, School of Medicine, Johns Hopkins University, Baltimore, MD 21205.
SuFey OngW. Harry Feinstone Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD 21205.
Djahida BedjaDepartment of Medicine, Division of Cardiology, School of Medicine, Johns Hopkins University, Baltimore, MD 21205.ORCID 0000-0002-1685-1083
Allison G HaysDepartment of Medicine, Division of Cardiology, School of Medicine, Johns Hopkins University, Baltimore, MD 21205.
Nisha A GilotraDepartment of Medicine, Division of Cardiology, School of Medicine, Johns Hopkins University, Baltimore, MD 21205.
Isabelle CoppensW. Harry Feinstone Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD 21205.
Noel R RoseW. Harry Feinstone Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD 21205.
Daniela ČihákováW. Harry Feinstone Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD 21205 dcihako1@jhmi.edu.ORCID 0000-0002-8713-2860
Johns Hopkins University · US

Funding

Myeloid Cells are Critical in Inflammatory Heart DiseaseR01HL118183 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI CIHAKOVA, DANIELA · 2014 to 2023
$4.4M
Eosinophilic MyocarditisR01HL113008 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI CIHAKOVA, DANIELA · 2012 to 2015
$1.6M
NHLBI NIH HHS R01 HL113008NHLBI NIH HHS R01 HL118183
6 · The paper itself

Abstract

Inflammatory dilated cardiomyopathy (DCMi) is a major cause of heart failure in children and young adults. DCMi develops in up to 30% of myocarditis patients, but the mechanisms involved in disease progression are poorly understood. Patients with eosinophilia frequently develop cardiomyopathies. In this study, we used the experimental autoimmune myocarditis (EAM) model to determine the role of eosinophils in myocarditis and DCMi. Eosinophils were dispensable for myocarditis induction but were required for progression to DCMi. Eosinophil-deficient ΔdblGATA1 mice, in contrast to WT mice, showed no signs of heart failure by echocardiography. Induction of EAM in hypereosinophilic IL-5Tg mice resulted in eosinophilic myocarditis with severe ventricular and atrial inflammation, which progressed to severe DCMi. This was not a direct effect of IL-5, as IL-5TgΔdblGATA1 mice were protected from DCMi, whereas IL-5

Indexed as

AnimalsAutoimmune DiseasesCardiomyopathy, DilatedDisease ProgressionEosinophilsFibrosisHumansInterferon-gammaInterleukin-13Interleukin-17Interleukin-4Interleukin-5MiceMice, Inbred BALB CMyocarditisInterferon-gammaInterleukin-13Interleukin-17Interleukin-4Interleukin-5

Identifiers

PMID28302646
PMCPMC5379983
OpenAlexW2597053455

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.