Evidence map›Paper›PMID 29769710›Full record

ArticleScientific reports2018

JDP2 overexpression provokes cardiac dysfunction in mice.

Jacqueline Heger, Julia Bornbaum, Alona Würfel, Christian Hill, Nils Brockmann, Renáta Gáspár, János Pálóczi, Zoltán V Varga, Márta Sárközy, Péter Bencsik and 9 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.7field-weighted citation impact, top 14% 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

14 citing papers in PubMed, 20 citations in OpenAlex.

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  9. JDP2, a Novel Molecular Key in Heart Failure and Atrial Fibrillation?International journal of molecular sciences · 2021
    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

19 authors at 5 institutions in 2 countries.

Jacqueline HegerInstitute of Physiology, Justus Liebig University, Giessen, Germany.
Julia BornbaumInstitute of Physiology, Justus Liebig University, Giessen, Germany.
Alona WürfelInstitute of Physiology, Justus Liebig University, Giessen, Germany.
Christian HillInstitute of Physiology, Justus Liebig University, Giessen, Germany.
Nils BrockmannInstitute of Physiology, Justus Liebig University, Giessen, Germany.
Renáta GáspárDepartment of Biochemistry, University of Szeged, Szeged, Hungary.
János PálócziDepartment of Biochemistry, University of Szeged, Szeged, Hungary.
Zoltán V VargaDepartment of Biochemistry, University of Szeged, Szeged, Hungary.
Márta SárközyDepartment of Biochemistry, University of Szeged, Szeged, Hungary.
Péter BencsikDepartment of Biochemistry, University of Szeged, Szeged, Hungary.
Tamás CsontDepartment of Biochemistry, University of Szeged, Szeged, Hungary.
Szilvia TörökDepartment of Biochemistry, University of Szeged, Szeged, Hungary.
Baktybek KojonazarovUniversities of Giessen and Marburg Lung Center (UGMLC), Excellence Cluster Cardio-Pulmonary System (ECCPS), Member of the German Center for Lung Research (DZL), Giessen, Germany.
Ralph Theo SchermulyUniversities of Giessen and Marburg Lung Center (UGMLC), Excellence Cluster Cardio-Pulmonary System (ECCPS), Member of the German Center for Lung Research (DZL), Giessen, Germany.
Kerstin BönglerInstitute of Physiology, Justus Liebig University, Giessen, Germany.
Mariana ParahulevaInternal Medicine/Cardiology and Angiology, University Hospital of Giessen and Marburg, Location Marburg, Marburg, Germany.
Peter FerdinandyDepartment of Biochemistry, University of Szeged, Szeged, Hungary.ORCID 0000-0002-6424-6806
Rainer SchulzInstitute of Physiology, Justus Liebig University, Giessen, Germany.
Gerhild EulerInstitute of Physiology, Justus Liebig University, Giessen, Germany. Gerhild.Euler@physiologie.med.uni-giessen.de.
Justus-Liebig-Universität Gießen · DEUniversity of Szeged · HUGerman Center for Lung Research · DESemmelweis University · HUUniversitätsklinikum Gießen und Marburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transcriptional regulator JDP2 (Jun dimerization protein 2) has been identified as a prognostic marker for patients to develop heart failure after myocardial infarction. We now performed in vivo studies on JDP2-overexpressing mice, to clarify the impact of JDP2 on heart failure progression. Therefore, during birth up to the age of 4 weeks cardiac-specific JDP2 overexpression was prevented by doxycycline feeding in transgenic mice. Then, JDP2 overexpression was started. Already after 1 week, cardiac function, determined by echocardiography, decreased which was also resembled on the cardiomyocyte level. After 5 weeks blood pressure declined, ejection fraction and cardiac output was reduced and left ventricular dilatation developed. Heart weight/body weight, and mRNA expression of ANP, inflammatory marker genes, collagen and fibronectin increased. Collagen 1 protein expression increased, and fibrosis developed. As an additional sign of elevated extracellular matrix remodeling, matrix metalloproteinase 2 activity increased in JDP2 mice. Thus, JDP2 overexpression is deleterious to heart function in vivo. It can be concluded that JDP2 overexpression provokes cardiac dysfunction in adult mice that is accompanied by hypertrophy and fibrosis. Thus, induction of JDP2 is a maladaptive response contributing to heart failure development.

Indexed as

AnimalsCardiomegalyCells, CulturedFibrosisHeart FailureMiceMice, Inbred C57BLMyocardial InfarctionMyocytes, CardiacRepressor ProteinsJundp2 protein, mouseRepressor Proteins

Identifiers

PMID29769710
PMCPMC5955919
OpenAlexW2805004408

What OpenQuestion holds

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LicenceCC BY
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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.