Evidence map›Paper›PMID 19920350›Full record

ArticleThe Journal of clinical investigation2009

Cardiac macrophage migration inhibitory factor inhibits JNK pathway activation and injury during ischemia/reperfusion.

Dake Qi, Xiaoyue Hu, Xiaohong Wu, Melanie Merk, Lin Leng, Richard Bucala, Lawrence H Young

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed, 1 pooled it
3.7field-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

102 citing papers in PubMed, 1 synthesis or guideline pooled it, 173 citations in OpenAlex.

  1. Myocardial Immune Cells: The Basis of Cardiac Immunology.Journal of immunology (Baltimore, Md. : 1950) · 2023
    Pooled it
  2. Article
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  8. Review
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  10. Review
  11. CD74 is a functional MIF receptor on activated CD4Cellular and molecular life sciences : CMLS · 2024
    Article
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  15. Article
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  17. Article
  18. Review
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  20. Article

42 more citing papers are in PubMed but not listed here.

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

7 authors at 1 institution in 1 country.

Dake QiSection of Cardiovascular Medicine, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut, USA.
Xiaoyue Hu
Xiaohong Wu
Melanie Merk
Lin Leng
Richard Bucala
Lawrence H Young
Yale University · US

Funding

REGULATION OF GLUCOSE TRANSPORT IN THE ISCHEMIC HEARTR01HL063811 · NHLBI · YALE UNIVERSITY · PI YOUNG, LAWRENCE H · 2000 to 2012
$4.4M
NHLBI NIH HHS R01 HL063811NHLBI NIH HHS R01 HL-63811PHS HHS A1043210
6 · The paper itself

Abstract

Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine that also modulates physiologic cell signaling pathways. MIF is expressed in cardiomyocytes and limits cardiac injury by enhancing AMPK activity during ischemia. Reperfusion injury is mediated in part by activation of the stress kinase JNK, but whether MIF modulates JNK in this setting is unknown. We examined the role of MIF in regulating JNK activation and cardiac injury during experimental ischemia/reperfusion in mouse hearts. Isolated perfused Mif-/- hearts had greater contractile dysfunction, necrosis, and JNK activation than WT hearts, with increased upstream MAPK kinase 4 phosphorylation, following ischemia/reperfusion. These effects were reversed if recombinant MIF was present during reperfusion, indicating that MIF deficiency during reperfusion exacerbated injury. Activated JNK acts in a proapoptotic manner by regulating BCL2-associated agonist of cell death (BAD) phosphorylation, and this effect was accentuated in Mif-/- hearts after ischemia/reperfusion. Similar detrimental effects of MIF deficiency were observed in vivo following coronary occlusion and reperfusion in Mif-/- mice. Importantly, excess JNK activation also was observed after hypoxia-reoxygenation in human fibroblasts homozygous for the MIF allele with the lowest level of promoter activity. These data indicate that endogenous MIF inhibits JNK pathway activation during reperfusion and protects the heart from injury. These findings have clinical implications for patients with the low-expression MIF allele.

Indexed as

AnimalsCell LineEnzyme ActivationHumansIntramolecular OxidoreductasesIn Vitro TechniquesJNK Mitogen-Activated Protein KinasesMacrophage Migration-Inhibitory FactorsMAP Kinase Kinase 4MiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutMyocardial ContractionMyocardial Reperfusion InjuryMyocardiumIntramolecular OxidoreductasesJNK Mitogen-Activated Protein Kinasesmacrophage migration inhibitory factor receptorMacrophage Migration-Inhibitory FactorsMAP Kinase Kinase 4Mif protein, mouseReceptors, Immunologic

Identifiers

PMID19920350
PMCPMC2786800
OpenAlexW2117810566

What OpenQuestion holds

Textmetadata
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.