Evidence map›Paper›PMID 28800592›Full record

ArticlePloS one2017

CX3CR1 knockout aggravates Coxsackievirus B3-induced myocarditis.

Irene Müller, Kathleen Pappritz, Konstantinos Savvatis, Kerstin Puhl, Fengquan Dong, Muhammad El-Shafeey, Nazha Hamdani, Isabell Hamann, Michel Noutsias, Carmen Infante-Duarte and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.2field-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

21 citing papers in PubMed, 51 citations in OpenAlex.

  1. Cardiomyocyte β-arrestins mediate inflammation and cGAS-STING activation in CVB3 viral myocarditis.American journal of physiology. Heart and circulatory physiology · 2026
    Article
  2. Review
  3. Review
  4. Alterations in CX3CL1 Levels and Its Role in Viral Pathogenesis.International journal of molecular sciences · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Chemokines in cardiac fibrosis.Current opinion in physiology · 2021
    Article
  13. A Toolbox of Potential Immune-Related Therapies for Inflammatory Cardiomyopathy.Journal of cardiovascular translational research · 2021
    Review
  14. Article
  15. Article
  16. Article
  17. Review
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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.

Irene MüllerCharité -Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Internal Medicine and Cardiology, Campus Virchow Klinikum, Berlin, Germany.ORCID http://orcid.org/0000-0001-8583-8985
Kathleen PappritzCharité -Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Internal Medicine and Cardiology, Campus Virchow Klinikum, Berlin, Germany.
Konstantinos SavvatisInherited Cardiovascular Diseases Unit, Barts Health NHS Trust, Barts Heart Centre, London, United Kingdom.
Kerstin PuhlCharité -Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Internal Medicine and Cardiology, Campus Virchow Klinikum, Berlin, Germany.
Fengquan DongCharité -Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Internal Medicine and Cardiology, Campus Virchow Klinikum, Berlin, Germany.
Muhammad El-ShafeeyCharité -Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Internal Medicine and Cardiology, Campus Virchow Klinikum, Berlin, Germany.
Nazha HamdaniDepartment of Cardiovascular Physiology, Ruhr University Bochum, Bochum, Germany.
Isabell HamannCharité -Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Institute for Medical Immunology, Campus Virchow Klinikum, Berlin, Germany.
Michel NoutsiasDepartment of Internal Medicine III, Division of Cardiology, Angiology and Intensive Medical Care, University Hospital Halle, Halle (Saale), Germany.
Carmen Infante-DuarteCharité -Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Institute for Medical Immunology, Campus Virchow Klinikum, Berlin, Germany.
Wolfgang A LinkeDepartment of Cardiovascular Physiology, Ruhr University Bochum, Bochum, Germany.
Sophie Van LinthoutCharité -Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Internal Medicine and Cardiology, Campus Virchow Klinikum, Berlin, Germany.
Carsten TschöpeCharité -Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Internal Medicine and Cardiology, Campus Virchow Klinikum, Berlin, Germany.
Humboldt-Universität zu Berlin · DERuhr University Bochum · DEBarts Health NHS Trust · GBUniversity Hospital in Halle · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Studies on inflammatory disorders elucidated the pivotal role of the CX3CL1/CX3CR1 axis with respect to the pathophysiology and diseases progression. Coxsackievirus B3 (CVB3)-induced myocarditis is associated with severe cardiac inflammation, which may progress to heart failure. We therefore investigated the influence of CX3CR1 ablation in the model of acute myocarditis, which was induced by inoculation with 5x105 plaque forming units of CVB3 (Nancy strain) in either CX3CR1-/- or C57BL6/j (WT) mice. Seven days after infection, myocardial inflammation, remodeling, and titin expression and phosphorylation were examined by immunohistochemistry, real-time PCR and Pro-Q diamond stain. Cardiac function was assessed by tip catheter. Compared to WT CVB3 mice, CX3CR1-/- CVB3 mice exhibited enhanced left ventricular expression of inflammatory cytokines and chemokines, which was associated with an increase of immune cell infiltration/presence. This shift towards a pro-inflammatory immune response further resulted in increased cardiac fibrosis and cardiomyocyte apoptosis, which was reflected by an impaired cardiac function in CX3CR1-/- CVB3 compared to WT CVB3 mice. These findings demonstrate a cardioprotective role of CX3CR1 in CVB3-infected mice and indicate the relevance of the CX3CL1/CX3CR1 system in CVB3-induced myocarditis.

Indexed as

AnimalsApoptosisCell Adhesion MoleculesChemokine CX3CL1Coxsackievirus InfectionsCX3C Chemokine Receptor 1Disease Models, AnimalEnterovirus B, HumanGene Expression RegulationHeart Function TestsHost-Pathogen InteractionsHumansInterleukinsMaleMiceMice, Inbred C57BLCell Adhesion MoleculesChemokine CX3CL1CX3C Chemokine Receptor 1Cx3cl1 protein, mouseCx3cr1 protein, mouseInterleukinsProtein KinasesReceptors, Chemokinetitin protein, mouse

Identifiers

PMID28800592
PMCPMC5553786
OpenAlexW2743785899

What OpenQuestion holds

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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.