Evidence map›Paper›PMID 37829205›Full record

ArticleiScience2023

Hypereosinophilia causes progressive cardiac pathologies in mice.

Nicola Laura Diny, Megan Kay Wood, Taejoon Won, Monica Vladut Talor, Clarisse Lukban, Djahida Bedja, Nadan Wang, Hannah Kalinoski, Abdel Daoud, C Conover Talbot and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in iScience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.7field-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

4 citing papers in PubMed, 7 citations in OpenAlex.

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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

12 authors at 1 institution in 1 country.

Nicola Laura DinyW. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD 21205, USA.
Megan Kay WoodW. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD 21205, USA.
Taejoon WonDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Monica Vladut TalorDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Clarisse LukbanDepartment of Cardiology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Djahida BedjaDepartment of Cardiology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Nadan WangDepartment of Cardiology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Hannah KalinoskiW. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD 21205, USA.
Abdel DaoudW. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD 21205, USA.
C Conover TalbotInstitute for Basic Biomedical Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Brian Leei LinDepartment of Cardiology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Daniela ČihákováW. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD 21205, USA.
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
Role of Sca-1+Cardiac Fibroblasts in Inflammatory Heart Disease`R01HL136586 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI CIHAKOVA, DANIELA · 2018 to 2021
$1.6M
The Role of Checkpoint inhibitors in CIAF31AR077406 · NIAMS · JOHNS HOPKINS UNIVERSITY · PI WOOD, MEGAN KAY · 2020 to 2022
$96k
NHLBI NIH HHS R01 HL118183NHLBI NIH HHS R01 HL136586NIAMS NIH HHS F31 AR077406Wellcome Trust
6 · The paper itself

Abstract

Hypereosinophilic syndrome is a progressive disease with extensive eosinophilia that results in organ damage. Cardiac pathologies are the main reason for its high mortality rate. A better understanding of the mechanisms of eosinophil-mediated tissue damage would benefit therapeutic development. Here, we describe the cardiac pathologies that developed in a mouse model of hypereosinophilic syndrome. These IL-5 transgenic mice exhibited decreased left ventricular function at a young age which worsened with age. Mechanistically, we demonstrated infiltration of activated eosinophils into the heart tissue that led to an inflammatory environment. Gene expression signatures showed tissue damage as well as repair and remodeling processes. Cardiomyocytes from IL-5Tg mice exhibited significantly reduced contractility relative to wild type (WT) controls. This impairment may result from the inflammatory stress experienced by the cardiomyocytes and suggest that dysregulation of contractility and Ca

Indexed as

Cell biologyMolecular biologyPhysiology

Identifiers

PMID37829205
PMCPMC10565781
OpenAlexW4386879935

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.