Evidence map›Paper›PMID 28615692›Full record

ArticleScientific reports2017

Wnt5a is associated with right ventricular dysfunction and adverse outcome in dilated cardiomyopathy.

Aurelija Abraityte, Ida G Lunde, Erik T Askevold, Annika E Michelsen, Geir Christensen, Pål Aukrust, Arne Yndestad, Arnt Fiane, Arne Andreassen, Svend Aakhus and 4 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Wnt5a-mediated Adipo-Cardiac Interorgan Communication in HFpEF.bioRxiv : the preprint server for biology · 2025
    Article
  4. Review
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  10. RBM20Journal of molecular and cellular cardiology · 2022
    Article
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  15. Article
  16. 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 1 institution in 2 countries.

Aurelija AbraityteResearch Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Ida G LundeCenter for Heart Failure Research, University of Oslo, Oslo, Norway.
Erik T AskevoldResearch Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Annika E MichelsenResearch Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Geir ChristensenCenter for Heart Failure Research, University of Oslo, Oslo, Norway.
Pål AukrustResearch Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Arne YndestadResearch Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Arnt FianeFaculty of Medicine, University of Oslo, Oslo, Norway.
Arne AndreassenDepartment of Cardiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Svend AakhusDepartment of Cardiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Christen P DahlResearch Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Lars GullestadFaculty of Medicine, University of Oslo, Oslo, Norway.
Kaspar BrochDepartment of Cardiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Thor UelandResearch Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway. thor.ueland@medisin.uio.no.
Oslo University Hospital · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Wingless (Wnt) pathway has been implicated in the pathogenesis of dilated cardiomyopathy (DCM). To explore the role of Wnt modulators Wnt5a and sFRP3 in DCM patients we analyzed the expression of Wnt5a and sFRP3 in plasma and myocardium of DCM patients and evaluated their effects on NFAT luciferase activity in neonatal mouse cardiomyocytes. Elevated circulating Wnt5a (n = 102) was associated with increased pulmonary artery pressures, decreased right ventricular function and adverse outcome, with a stronger association in more severely affected patients. A higher Wnt5a/sFRP3 ratio (n = 25) was found in the right ventricle vs. the left ventricle and was correlated with NFAT activation as well as pulmonary artery pressures. Wnt5a induced NFAT activation and sFRP3 release in cardiomyocytes in vitro, while sFRP3 antagonized Wnt5a. Wnt5a is associated with right ventricular dysfunction and adverse outcome in DCM patients and may promote the progression of DCM through NFAT signaling.

Indexed as

Adaptor Proteins, Signal TransducingAdverse Outcome PathwaysAnimalsCardiomyopathy, DilatedFemaleHumansKaplan-Meier EstimateMaleMiceMiddle AgedMuscle ProteinsNFATC Transcription FactorsSignal TransductionVentricular Dysfunction, RightWnt-5a ProteinAdaptor Proteins, Signal TransducingMuscle ProteinsMYOZ3 protein, humanNFATC Transcription FactorsWnt-5a ProteinWNT5A protein, human

Identifiers

PMID28615692
PMCPMC5471231
OpenAlexW2624251034

What OpenQuestion holds

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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.