Evidence map›Paper›PMID 27335054›Full record

ArticleCardiovascular drugs and therapy2016

Exogenous Administration of Recombinant MIF at Physiological Concentrations Failed to Attenuate Infarct Size in a Langendorff Perfused Isolated Mouse Heart Model.

Xavier Rossello, Niall Burke, Christian Stoppe, Jurgen Bernhagen, Sean M Davidson, Derek M Yellon

Open access · hybridAbstract read
In one paragraph

Article in Cardiovascular drugs and therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.0field-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

12 citing papers in PubMed, 19 citations in OpenAlex.

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  10. The role of PI3Kα isoform in cardioprotection.Basic research in cardiology · 2017
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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

6 authors at 3 institutions in 2 countries.

Xavier RosselloThe Hatter Cardiovascular Institute, University College London, 67 Chenies Mews, London, WC1E 6HX 2, UK.
Niall BurkeThe Hatter Cardiovascular Institute, University College London, 67 Chenies Mews, London, WC1E 6HX 2, UK.
Christian StoppeDepartment of Intensive Care Medicine, University Hospital, Aachen, RWTH, Germany.
Jurgen BernhagenVascular Biology, Institute for Stroke and Dementia Research, Klinikum der Universität München, Ludwig-Maximilians-University, 81377, Munich, Germany.
Sean M DavidsonThe Hatter Cardiovascular Institute, University College London, 67 Chenies Mews, London, WC1E 6HX 2, UK.
Derek M YellonThe Hatter Cardiovascular Institute, University College London, 67 Chenies Mews, London, WC1E 6HX 2, UK. d.yellon@ucl.ac.uk.
University College London · GBLudwig-Maximilians-Universität München · DERWTH Aachen University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeEvidence suggests a two-pronged role of endogenous macrophage migration inhibitory factor (MIF) release in ischemia/reperfusion injury. We aimed to assess whether its exogenous administration confers cardioprotection.

methodsMale C57/BL6 mice were randomly allocated to receive recombinant mouse MIF (rMIF) at physiological (ng/mL) concentrations in a dose-response fashion before or after a protocol of 35 min of ischemia and 2 h of reperfusion in an isolated Langendorff-perfused model with infarct size as endpoint. Isolated primary cardiomyocytes were also used for cell survival studies using rMIF at a supra-physiological concentration of 1 μg/mL. Pro-survival kinase activation was also studied using Western blot analyses.

resultsExogenous MIF did not elicit a cardioprotective effect either when administered before the ischemic insult or when applied at reperfusion. rMIF did not confer protection when it was applied immediately before or after a hypoxia/reoxygenation insult in primary isolated cardiomyocytes. Consistently, hearts treated with MIF did not show a significant increase in phosphorylated Akt and ERK1/2.

conclusionThe exogenous administration of rMIF in a physiological concentration range both before ischemia and at reperfusion did not show cardioprotective effects. Although these results do not address the role of endogenous MIF after an ischemic insult followed by reperfusion, they may limit the potential translational value of rMIF.

Indexed as

AnimalsCell SurvivalExtracellular Signal-Regulated MAP KinasesIntramolecular OxidoreductasesIn Vitro TechniquesIschemic Preconditioning, MyocardialMacrophage Migration-Inhibitory FactorsMaleMice, Inbred C57BLMyocardial InfarctionMyocardial Reperfusion InjuryMyocardiumMyocytes, CardiacPerfusionPhosphorylationProto-Oncogene Proteins c-aktExtracellular Signal-Regulated MAP KinasesIntramolecular OxidoreductasesMacrophage Migration-Inhibitory FactorsMif protein, mouseProto-Oncogene Proteins c-aktRecombinant ProteinsIschemia–reperfusionIschemic preconditioningMacrophage migration inhibitory factorMyocardial infarction

Identifiers

PMID27335054
PMCPMC5055564
OpenAlexW2469020466

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.