Evidence map›Paper›PMID 27936014›Full record

ArticlePloS one2016

Inhibition of Interleukin-6 Receptor in a Murine Model of Myocardial Ischemia-Reperfusion.

Minke H T Hartman, Inge Vreeswijk-Baudoin, Hilde E Groot, Kees W A van de Kolk, Rudolf A de Boer, Irene Mateo Leach, Rozemarijn Vliegenthart, Herman H W Sillje, Pim van der Harst

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 2 pooled it
3.8field-weighted citation impact, top 6% 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

30 citing papers in PubMed, 2 syntheses or guidelines pooled it, 43 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

9 authors at 1 institution in 1 country.

Minke H T HartmanUniversity of Groningen, University Medical Center Groningen, the department of Cardiology, Groningen, the Netherlands.ORCID http://orcid.org/0000-0002-6965-3259
Inge Vreeswijk-BaudoinUniversity of Groningen, University Medical Center Groningen, the department of Cardiology, Groningen, the Netherlands.
Hilde E GrootUniversity of Groningen, University Medical Center Groningen, the department of Cardiology, Groningen, the Netherlands.
Kees W A van de KolkUniversity of Groningen, University Medical Center Groningen, the Central Animal Facility, Groningen, the Netherlands.
Rudolf A de BoerUniversity of Groningen, University Medical Center Groningen, the department of Cardiology, Groningen, the Netherlands.
Irene Mateo LeachUniversity of Groningen, University Medical Center Groningen, the department of Cardiology, Groningen, the Netherlands.
Rozemarijn VliegenthartUniversity of Groningen, University Medical Center Groningen, the department of Radiology, Groningen, the Netherlands.
Herman H W SilljeUniversity of Groningen, University Medical Center Groningen, the department of Cardiology, Groningen, the Netherlands.
Pim van der HarstUniversity of Groningen, University Medical Center Groningen, the department of Cardiology, Groningen, the Netherlands.
University Medical Center Groningen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInterleukin-6 (IL-6) levels are upregulated in myocardial infarction. Recent data suggest a causal role of the IL-6 receptor (IL-6R) in coronary heart disease. We evaluated if IL-6R blockade by a monoclonal antibody (MR16-1) prevents the heart from adverse left ventricular remodeling in a mouse model of ischemia-reperfusion (I/R).

methodsCJ57/BL6 mice underwent I/R injury (left coronary artery ligation for 45 minutes) or sham surgery, and thereafter received MR16-1 (2mg/mouse) 5 minutes before reperfusion and 0.5mg/mouse weekly during four weeks, or control IgG treatment. Cardiac Magnetic Resonance Imaging (CMR) and hemodynamic measurements were performed to determine cardiac function after four weeks.

resultsI/R caused left ventricular dilatation and a decrease in left ventricular ejection fraction (LVEF). However, LVEF was significantly lower in the MR16-1 treatment group compared to the IgG group (28±4% vs. 35±6%, p = 0.02; sham 45±6% vs. 43±4%, respectively; p = NS). Cardiac relaxation (assessed by dP/dT) was not significantly different between the MR16-1 and IgG groups. Also, no differences were observed in histological myocardial fibrosis, infarct size and myocyte hypertrophy between the groups.

conclusionBlockade of the IL-6R receptor by the monoclonal MR16-1 antibody for four weeks started directly after I/R injury did not prevent the process of cardiac remodeling in mice, but rather associated with a deterioration in the process of adverse cardiac remodeling.

Indexed as

AnimalsAntibodies, MonoclonalDisease Models, AnimalFibrosisHeartHemodynamicsHypertrophyInterleukin-6MaleMice, Inbred C57BLMicroscopy, FluorescenceMyocardial InfarctionMyocardial Reperfusion InjuryMyocardiumReceptors, Interleukin-6Time FactorsAntibodies, MonoclonalInterleukin-6Receptors, Interleukin-6

Identifiers

PMID27936014
PMCPMC5147868
OpenAlexW2559799386

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.