Evidence map›Paper›PMID 29344292›Full record

ReviewTheranostics2018

Galectin-3 Activation and Inhibition in Heart Failure and Cardiovascular Disease: An Update.

Navin Suthahar, Wouter C Meijers, Herman H W Silljé, Jennifer E Ho, Fu-Tong Liu, Rudolf A de Boer

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Theranostics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 158 papers, 9 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
158citing papers in PubMed, 9 pooled it
7.3field-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

158 citing papers in PubMed, 9 syntheses or guidelines pooled it, 301 citations in OpenAlex.

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  5. Right Heart Function in Cardiorenal Syndrome.Current heart failure reports · 2022
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98 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

6 authors at 3 institutions in 3 countries.

Navin SuthaharUniversity Medical Center Groningen, University of Groningen, Department of Cardiology, PO Box 30.001, 9700 RB Groningen, the Netherlands.
Wouter C MeijersUniversity Medical Center Groningen, University of Groningen, Department of Cardiology, PO Box 30.001, 9700 RB Groningen, the Netherlands.
Herman H W SilljéUniversity Medical Center Groningen, University of Groningen, Department of Cardiology, PO Box 30.001, 9700 RB Groningen, the Netherlands.
Jennifer E HoMassachusetts General Hospital, Cardiovascular Research Center, Boston, MA, USA.
Fu-Tong LiuInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
Rudolf A de BoerUniversity Medical Center Groningen, University of Groningen, Department of Cardiology, PO Box 30.001, 9700 RB Groningen, the Netherlands.
University Medical Center Groningen · NLUniversity of Groningen · NLMassachusetts General Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Galectin-3 is a versatile protein orchestrating several physiological and pathophysiological processes in the human body. In the last decade, considerable interest in galectin-3 has emerged because of its potential role as a biotarget. Galectin-3 is differentially expressed depending on the tissue type, however its expression can be induced under conditions of tissue injury or stress. Galectin-3 overexpression and secretion is associated with several diseases and is extensively studied in the context of fibrosis, heart failure, atherosclerosis and diabetes mellitus. Monomeric (extracellular) galectin-3 usually undergoes further "activation" which significantly broadens the spectrum of biological activity mainly by modifying its carbohydrate-binding properties. Self-interactions of this protein appear to play a crucial role in regulating the extracellular activities of this protein, however there is limited and controversial data on the mechanisms involved. We therefore summarize (recent) literature in this area and describe galectin-3 from a binding perspective providing novel insights into mechanisms by which galectin-3 is known to be "activated" and how such activation may be regulated in pathophysiological scenarios.

Indexed as

AnimalsAtherosclerosisDiabetes Mellitus, Type 2Galectin 3Heart FailureHumansGalectin 3carbohydrate binding domaincardiovascular diseasecell-cell adhesionextracellular matrixfibrosisGalectin-3heart failureinteractionrenal disease

Identifiers

PMID29344292
PMCPMC5771079
OpenAlexW2769708180

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.