Evidence map›Paper›PMID 25725809›Full record

ArticleBasic research in cardiology2015

Exendin-4 protects against post-myocardial infarction remodelling via specific actions on inflammation and the extracellular matrix.

Emma Robinson, Roslyn S Cassidy, Mitchel Tate, Youyou Zhao, Samuel Lockhart, Danielle Calderwood, Rachel Church, Mary K McGahon, Derek P Brazil, Barbara J McDermott and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Basic research in cardiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 3 pooled it
6.9field-weighted citation impact, top 2% 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

42 citing papers in PubMed, 3 syntheses or guidelines pooled it, 67 citations in OpenAlex.

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  16. Gut Molecules in Cardiometabolic Diseases: The Mechanisms behind the Story.International journal of molecular sciences · 2023
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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

12 authors at 1 institution in 1 country.

Emma RobinsonCentre for Experimental Medicine, Institute of Clinical Science Block A, Queen's University Belfast, Grosvenor Road, Belfast, BT12 6BA, UK.
Roslyn S Cassidy
Mitchel Tate
Youyou Zhao
Samuel Lockhart
Danielle Calderwood
Rachel Church
Mary K McGahon
Derek P Brazil
Barbara J McDermott
Brian D Green
David J Grieve
Queen's University Belfast · GB

Funding

British Heart Foundation FS/11/36/28872British Heart Foundation PG/09/102British Heart Foundation PG/09/102/28133Medical Research Council G0601215
6 · The paper itself

Abstract

Glucagon-like peptide-1 (GLP-1) is an insulin-releasing hormone clinically exploited for glycaemic control in diabetes, which also confers acute cardioprotection and benefits in experimental/clinical heart failure. We specifically investigated the role of the GLP-1 mimetic, exendin-4, in post-myocardial infarction (MI) remodelling, which is a key contributor to heart failure. Adult female normoglycaemic mice underwent coronary artery ligation/sham surgery prior to infusion with exendin-4/vehicle for 4 weeks. Metabolic parameters and infarct sizes were comparable between groups. Exendin-4 protected against cardiac dysfunction and chamber dilatation post-MI and improved survival. Furthermore, exendin-4 modestly decreased cardiomyocyte hypertrophy/apoptosis but markedly attenuated interstitial fibrosis and myocardial inflammation post-MI. This was associated with altered extracellular matrix (procollagen IαI/IIIαI, connective tissue growth factor, fibronectin, TGF-β3) and inflammatory (IL-10, IL-1β, IL-6) gene expression in exendin-4-treated mice, together with modulation of both Akt/GSK-3β and Smad2/3 signalling. Exendin-4 also altered macrophage response gene expression in the absence of direct actions on cardiac fibroblast differentiation, suggesting cardioprotective effects occurring secondary to modulation of inflammation. Our findings indicate that exendin-4 protects against post-MI remodelling via preferential actions on inflammation and the extracellular matrix independently of its established actions on glycaemic control, thereby suggesting that selective targeting of GLP-1 signalling may be required to realise its clear therapeutic potential for post-MI heart failure.

Indexed as

AnimalsBlotting, WesternDisease Models, AnimalExenatideExtracellular MatrixFemaleImmunohistochemistryInflammationIn Situ Nick-End LabelingMiceMice, Inbred C57BLMyocardial InfarctionPeptidesRatsReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionExenatidePeptidesVenoms

Identifiers

PMID25725809
PMCPMC4344953
OpenAlexW2110544922

What OpenQuestion holds

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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.