Evidence map›Paper›PMID 23753877›Full record

ArticleCirculation2013

Limiting cardiac ischemic injury by pharmacological augmentation of macrophage migration inhibitory factor-AMP-activated protein kinase signal transduction.

Jingying Wang, Chao Tong, Xiaoyan Yan, Eddie Yeung, Sunilkumar Gandavadi, Alissa A Hare, Xin Du, Yibang Chen, Huabao Xiong, Changxing Ma and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Circulation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.0field-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

48 citing papers in PubMed, 89 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

15 authors at 1 institution in 1 country.

Jingying WangDepartment of Pharmacology and Toxicology, State University of New York at Buffalo, Buffalo, NY 14214-3000, USA.
Chao Tong
Xiaoyan Yan
Eddie Yeung
Sunilkumar Gandavadi
Alissa A Hare
Xin Du
Yibang Chen
Huabao Xiong
Changxing Ma
Lin Leng
Lawrence H Young
William L Jorgensen
Ji Li
Richard Bucala
Yale University · US

Funding

POTENTIAL FUNCTIONS FOR WATER PROTEIN INTERACTIONSR01GM032136 · NIGMS · YALE UNIVERSITY · PI JORGENSEN, WILLIAM L. · 1985 to 2023
$8.2M
REGULATION OF GLUCOSE TRANSPORT IN THE ISCHEMIC HEARTR01HL063811 · NHLBI · YALE UNIVERSITY · PI YOUNG, LAWRENCE H · 2000 to 2012
$4.4M
MIF AND THE HOST RESPONSE TO INFECTIONR01AI042310 · NIAID · YALE UNIVERSITY · PI BUCALA, RICHARD J · 1998 to 2013
$4.3M
MIF and Host Response to InfectionR56AI042310 · NIAID · YALE UNIVERSITY · PI BUCALA, RICHARD J · 2014 to 2014
$426k
NHLBI NIH HHS HL063811NHLBI NIH HHS R01 HL063811NIAID NIH HHS AI042310NIAID NIH HHS R01 AI042310NIAID NIH HHS R56 AI042310NIGMS NIH HHS GM032136NIGMS NIH HHS R01 GM032136
6 · The paper itself

Abstract

backgroundMacrophage migration inhibitory factor (MIF) exerts a protective effect on ischemic myocardium by activating AMP-activated protein kinase (AMPK). Small molecules that increase the affinity of MIF for its receptor have been recently designed, and we hypothesized that such agonists may enhance AMPK activation and limit ischemic tissue injury. METHODS AND

resultsTreatment of cardiomyocytes with the candidate MIF agonist, MIF20, augmented AMPK phosphorylation, increased by 50% the surface localization of glucose transporter, and enhanced by 25% cellular glucose uptake in comparison with MIF alone. In mouse hearts perfused with MIF20 before no-flow ischemia and reperfusion, postischemic left ventricular function improved commensurately with an increase in cardiac MIF-AMPK activation and an augmentation in myocardial glucose uptake. By contrast, small-molecule MIF agonism was not effective in cells or tissues genetically deficient in MIF or the MIF receptor, verifying the specificity of MIF20 for MIF-dependent AMPK signaling. The protective effect of MIF20 also was evident in an in vivo regional ischemia model. Mice treated with MIF20 followed by left coronary artery occlusion and reperfusion showed a significant reduction in infarcted myocardium.

conclusionsThese data support the pharmacological utility of small-molecule MIF agonists in enhancing AMPK activation and reducing cardiac ischemic injury.

Indexed as

AMP-Activated Protein KinasesAnimalsAntigens, Differentiation, B-LymphocyteCardiotonic AgentsCells, CulturedGlucoseHistocompatibility Antigens Class IIIntramolecular OxidoreductasesIsoxazolesMacrophage Migration-Inhibitory FactorsMaleMiceMice, Inbred C57BLMice, KnockoutMyocardial InfarctionMyocardial Ischemia3-(4-hydroxyphenyl)-4,5-dihydro-5-isoxazoleacetic acid methyl esterAMP-Activated Protein KinasesAntigens, Differentiation, B-LymphocyteCardiotonic AgentsGlucoseHistocompatibility Antigens Class IIIntramolecular Oxidoreductasesinvariant chainIsoxazolesMacrophage Migration-Inhibitory FactorsMif protein, mouseRecombinant Proteinsglucose transporterischemiamigration inhibitory factor agonist

Identifiers

PMID23753877
PMCPMC3781594
OpenAlexW2057846421

What OpenQuestion holds

Textmetadata
LicenceTDM
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.