Evidence map›Paper›PMID 29844319›Full record

ArticleScientific reports2018

Mechanisms responsible for increased circulating levels of galectin-3 in cardiomyopathy and heart failure.

My-Nhan Nguyen, Yidan Su, Donna Vizi, Lu Fang, Andris H Ellims, Wei-Bo Zhao, Helen Kiriazis, Xiao-Ming Gao, Junichi Sadoshima, Andrew J Taylor and 4 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

35 citing papers in PubMed, 58 citations in OpenAlex.

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  8. Inflammation in heart failure: pathophysiology and therapeutic strategies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Review
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  10. Article
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  15. Protection of CAPE-pNOInflammation · 2022
    Article
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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

14 authors at 5 institutions in 3 countries.

My-Nhan NguyenBaker Heart and Diabetes Institute, Melbourne, Australia.
Yidan SuBaker Heart and Diabetes Institute, Melbourne, Australia.
Donna ViziDepartment of Cardiovascular Medicine, the Alfred Hospital, Melbourne, Australia.
Lu FangBaker Heart and Diabetes Institute, Melbourne, Australia.
Andris H EllimsDepartment of Cardiovascular Medicine, the Alfred Hospital, Melbourne, Australia.
Wei-Bo ZhaoBaker Heart and Diabetes Institute, Melbourne, Australia.
Helen KiriazisBaker Heart and Diabetes Institute, Melbourne, Australia.
Xiao-Ming GaoBaker Heart and Diabetes Institute, Melbourne, Australia.
Junichi SadoshimaDepartment of Cell Biology and Molecular Medicine Rutgers, New Jersey Medical School, New Jersey, USA.
Andrew J TaylorDepartment of Cardiovascular Medicine, the Alfred Hospital, Melbourne, Australia.
Julie R McMullenBaker Heart and Diabetes Institute, Melbourne, Australia.
Anthony M DartBaker Heart and Diabetes Institute, Melbourne, Australia.
David M KayeBaker Heart and Diabetes Institute, Melbourne, Australia.
Xiao-Jun DuBaker Heart and Diabetes Institute, Melbourne, Australia. xiao-jun.du@baker.edu.au.
Baker Heart and Diabetes Institute · AUThe Alfred Hospital · AUMonash University · AUArmy Medical University · CNRutgers, The State University of New Jersey · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Galectin-3 is a biomarker of heart disease. However, it remains unknown whether increase in galectin-3 levels is dependent on aetiology or disease-associated conditions and whether diseased heart releases galectin-3 into the circulation. We explored these questions in mouse models of heart disease and in patients with cardiomyopathy. All mouse models (dilated cardiomyopathy, DCM; fibrotic cardiomyopathy, ischemia-reperfusion, I/R; treatment with β-adrenergic agonist isoproterenol) showed multi-fold increases in cardiac galectin-3 expression and preserved renal function. In mice with fibrotic cardiomyopathy, I/R or isoproterenol treatment, plasma galectin-3 levels and density of cardiac inflammatory cells were elevated. These models also exhibited parallel changes in cardiac and plasma galectin-3 levels and presence of trans-cardiac galectin-3 gradient, indicating cardiac release of galectin-3. DCM mice showed no change in circulating galectin-3 levels nor trans-cardiac galectin-3 gradient or myocardial inflammatory infiltration despite a 50-fold increase in cardiac galectin-3 content. In patients with hypertrophic cardiomyopathy or DCM, plasma galectin-3 increased only in those with renal dysfunction and a trans-cardiac galectin-3 gradient was not present. Collectively, this study documents the aetiology-dependency and diverse mechanisms of increment in circulating galectin-3 levels. Our findings highlight cardiac inflammation and enhanced β-adrenoceptor activation in mediating elevated galectin-3 levels via cardiac release in the mechanism.

Indexed as

AdultAnimalsBlood ProteinsCardiomyopathiesCohort StudiesDisease Models, AnimalFemaleGalectin 3GalectinsHeart FailureHumansInflammationMaleMiceMiddle AgedReceptors, Adrenergic, betaBlood ProteinsGalectin 3GalectinsLGALS3 protein, humanReceptors, Adrenergic, beta

Identifiers

PMID29844319
PMCPMC5973942
OpenAlexW2805313934

What OpenQuestion holds

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LicenceCC BY
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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.