Evidence map›Paper›PMID 30797757›Full record

ArticleDevelopmental biology2019

The Wnt inhibitor Dkk1 is required for maintaining the normal cardiac differentiation program in Xenopus laevis.

Yanchun Guo, Tatjana Dorn, Susanne J Kühl, Alexander Linnemann, Melanie Rothe, Astrid S Pfister, Seppo Vainio, Karl-Ludwig Laugwitz, Alessandra Moretti, Michael Kühl

Open access · hybridAbstract read
In one paragraph

Article in Developmental biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

9 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
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  3. Inflammation and DKK1-induced AKT activation contribute to endothelial dysfunction following NR2F2 loss.American journal of physiology. Lung cellular and molecular physiology · 2023
    Article
  4. Review
  5. Review
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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

10 authors at 4 institutions in 2 countries.

Yanchun GuoInstitute for Biochemistry and Molecular Biology, Ulm University, Albert-Einstein-Allee 11, 89081 Ulm, Germany; International Graduate School in Molecular Medicine Ulm, Ulm University, 89081 Ulm, Germany.
Tatjana DornKlinik und Poliklinik für Innere Medizin I, Klinikum Rechts der Isar der Technischen Universität München, Ismaninger Strasse 22, 81675 Munich, Germany.
Susanne J KühlInstitute for Biochemistry and Molecular Biology, Ulm University, Albert-Einstein-Allee 11, 89081 Ulm, Germany.
Alexander LinnemannInstitute for Biochemistry and Molecular Biology, Ulm University, Albert-Einstein-Allee 11, 89081 Ulm, Germany.
Melanie RotheInstitute for Biochemistry and Molecular Biology, Ulm University, Albert-Einstein-Allee 11, 89081 Ulm, Germany; International Graduate School in Molecular Medicine Ulm, Ulm University, 89081 Ulm, Germany.
Astrid S PfisterInstitute for Biochemistry and Molecular Biology, Ulm University, Albert-Einstein-Allee 11, 89081 Ulm, Germany.
Seppo VainioFaculty of Biochemistry and Molecular Medicine, Biocenter Oulu, InfoTech Oulu, Oulu University and Biobank Borealis of Northern Finland, Oulu University Hospital, Aapistie 5, FIN-90014, University of Oulu, Finland.
Karl-Ludwig LaugwitzKlinik und Poliklinik für Innere Medizin I, Klinikum Rechts der Isar der Technischen Universität München, Ismaninger Strasse 22, 81675 Munich, Germany; DZHK (German Centre for Cardiovascular Research) - Partner Site Munich Heart Alliance, Munich, Germany.
Alessandra MorettiKlinik und Poliklinik für Innere Medizin I, Klinikum Rechts der Isar der Technischen Universität München, Ismaninger Strasse 22, 81675 Munich, Germany; DZHK (German Centre for Cardiovascular Research) - Partner Site Munich Heart Alliance, Munich, Germany. Electronic address: amoretti@mytum.de.
Michael KühlInstitute for Biochemistry and Molecular Biology, Ulm University, Albert-Einstein-Allee 11, 89081 Ulm, Germany. Electronic address: michael.kuehl@uni-ulm.de.
Universität Ulm · DEKlinikum rechts der Isar · DEGerman Centre for Cardiovascular Research · DEUniversity of Oulu · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Wnt proteins can activate different intracellular signaling pathways. These pathways need to be tightly regulated for proper cardiogenesis. The canonical Wnt/β-catenin inhibitor Dkk1 has been shown to be sufficient to trigger cardiogenesis in gain-of-function experiments performed in multiple model systems. Loss-of-function studies however did not reveal any fundamental function for Dkk1 during cardiogenesis. Using Xenopus laevis as a model we here show for the first time that Dkk1 is required for proper differentiation of cardiomyocytes, whereas specification of cardiomyocytes remains unaffected in absence of Dkk1. This effect is at least in part mediated through regulation of non-canonical Wnt signaling via Wnt11. In line with these observations we also found that Isl1, a critical regulator for specification of the common cardiac progenitor cell (CPC) population, acts upstream of Dkk1.

Indexed as

Cell DifferentiationWnt Signaling PathwayAnimalsBiomarkersBody PatterningDigestive SystemDown-RegulationEmbryo, NonmammalianEndodermGene Expression Regulation, DevelopmentalIntercellular Signaling Peptides and ProteinsLIM-Homeodomain ProteinsMesodermMyocardiumMyocytes, CardiacOrganogenesisBiomarkersdkk1 protein, Xenopusinsulin gene enhancer binding protein Isl-1Intercellular Signaling Peptides and ProteinsLIM-Homeodomain ProteinsTranscription FactorsWnt ProteinsXenopus ProteinsCardiac differentiationdkk1isl1

Identifiers

PMID30797757
PMCPMC6496975
OpenAlexW2916994215

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.