Evidence map›Paper›PMID 30459442›Full record

ArticleScientific reports2018

IL-23R Signaling Plays No Role in Myocardial Infarction.

Erika Engelowski, Nastaran Fazel Modares, Simone Gorressen, Pascal Bouvain, Dominik Semmler, Christina Alter, Zhaoping Ding, Ulrich Flögel, Jürgen Schrader, Haifeng Xu and 4 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
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 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 45% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. 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

14 authors at 1 institution in 1 country.

Erika EngelowskiInstitute of Biochemistry and Molecular Biology II, Medical Faculty, Heinrich-Heine University, 40225, Düsseldorf, Germany.
Nastaran Fazel ModaresInstitute of Biochemistry and Molecular Biology II, Medical Faculty, Heinrich-Heine University, 40225, Düsseldorf, Germany.
Simone GorressenInstitute of Pharmacology and Clinical Pharmacology, Medical Faculty, Heinrich-Heine University, 40225, Düsseldorf, Germany.
Pascal BouvainInstitute for Molecular Cardiology, Medical Faculty, Heinrich-Heine University, 40225, Düsseldorf, Germany.
Dominik SemmlerInstitute of Pharmacology and Clinical Pharmacology, Medical Faculty, Heinrich-Heine University, 40225, Düsseldorf, Germany.
Christina AlterInstitute for Molecular Cardiology, Medical Faculty, Heinrich-Heine University, 40225, Düsseldorf, Germany.
Zhaoping DingInstitute for Molecular Cardiology, Medical Faculty, Heinrich-Heine University, 40225, Düsseldorf, Germany.
Ulrich FlögelInstitute for Molecular Cardiology, Medical Faculty, Heinrich-Heine University, 40225, Düsseldorf, Germany.
Jürgen SchraderInstitute for Molecular Cardiology, Medical Faculty, Heinrich-Heine University, 40225, Düsseldorf, Germany.
Haifeng XuInstitute of Molecular Medicine II, Medical Faculty, Heinrich-Heine-University, Düsseldorf, Germany.
Philipp A LangInstitute of Molecular Medicine II, Medical Faculty, Heinrich-Heine-University, Düsseldorf, Germany.
Jens FischerInstitute of Pharmacology and Clinical Pharmacology, Medical Faculty, Heinrich-Heine University, 40225, Düsseldorf, Germany.
Doreen M FlossInstitute of Biochemistry and Molecular Biology II, Medical Faculty, Heinrich-Heine University, 40225, Düsseldorf, Germany.
Jürgen SchellerInstitute of Biochemistry and Molecular Biology II, Medical Faculty, Heinrich-Heine University, 40225, Düsseldorf, Germany. jscheller@uni-duesseldorf.de.
Heinrich Heine University Düsseldorf · DE

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) SFB1116Deutsche Forschungsgemeinschaft (German Research Foundation) SFB974
6 · The paper itself

Abstract

Ischemic heart diseases are the most frequent diseases in the western world. Apart from Interleukin (IL-)1, inflammatory therapeutic targets in the clinic are still missing. Interestingly, opposing roles of the pro-inflammatory cytokine IL-23 have been described in cardiac ischemia in mice. IL-23 is a composite cytokine consisting of p19 and p40 which binds to IL-23R and IL-12Rβ1 to initiate signal transduction characterized by activation of the Jak/STAT, PI3K and Ras/Raf/MAPK pathways. Here, we generate IL-23R-Y416FΔICD signaling deficient mice and challenged these mice in close- and open-chest left anterior descending coronary arteria ischemia/reperfusion experiments. Our experiments showed only minimal changes in all assayed parameters in IL-23R signaling deficient mice compared to wild-type mice in ischemia and for up to four weeks of reperfusion, including ejection fraction, endsystolic volume, enddiastolic volume, infarct size, gene regulation and α smooth muscle actin (αSMA) and Hyaluronic acid (HA) protein expression. Moreover, injection of IL-23 in wild-type mice after LAD ischemia/reperfusion had also no influence on the outcome of the healing phase. Our data showed that IL-23R deficiency has no effects in myocardial I/R.

Indexed as

AnimalsGene Expression RegulationMaleMiceMice, Inbred C57BLMice, KnockoutMyocardial InfarctionMyocardial Reperfusion InjuryMyocardiumReceptors, InterleukinSignal Transductioninterleukin-23 receptor, mouseReceptors, Interleukin

Identifiers

PMID30459442
PMCPMC6244091
OpenAlexW2900745827

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.