Evidence map›Paper›PMID 32885664›Full record

ArticleCirculation2020

An Important Role for DNMT3A-Mediated DNA Methylation in Cardiomyocyte Metabolism and Contractility.

Alexandra Madsen, Grit Höppner, Julia Krause, Marc N Hirt, Sandra D Laufer, Michaela Schweizer, Wilson Lek Wen Tan, Diogo Mosqueira, Chukwuemeka George Anene-Nzelu, Ives Lim and 4 more

Erratum issuedOpen access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Circulation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

56 citing papers in PubMed, 80 citations in OpenAlex.

  1. Review
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  3. Cardiac epigenome in heart development and disease.Nature reviews. Cardiology · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 5 institutions in 4 countries.

Alexandra MadsenInstitute of Experimental Pharmacology and Toxicology (A.M., G.H., M.N.H., S.D.L., T.E., J.S.), University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Grit HöppnerInstitute of Experimental Pharmacology and Toxicology (A.M., G.H., M.N.H., S.D.L., T.E., J.S.), University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Julia KrauseDZHK (German Centre for Cardiovascular Research), partner site Hamburg/Kiel/Lübeck, Hamburg, Germany (A.M., G.H., J.K., M.N.H., S.D.L., T.E., J.S.).
Marc N HirtInstitute of Experimental Pharmacology and Toxicology (A.M., G.H., M.N.H., S.D.L., T.E., J.S.), University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Sandra D LauferInstitute of Experimental Pharmacology and Toxicology (A.M., G.H., M.N.H., S.D.L., T.E., J.S.), University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Michaela SchweizerDepartment of Morphology and Electron Microscopy, Center for Molecular Neurobiology (M.S.), University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Wilson Lek Wen TanGenome Institute of Singapore (W.L.W.T., C.G.A.-N., I.L., R.S.Y.F.).
Diogo MosqueiraDivision of Cancer & Stem Cells, Biodiscovery Institute, University of Nottingham, United Kingdom (D.M.).
Chukwuemeka George Anene-NzeluGenome Institute of Singapore (W.L.W.T., C.G.A.-N., I.L., R.S.Y.F.).
Ives LimGenome Institute of Singapore (W.L.W.T., C.G.A.-N., I.L., R.S.Y.F.).
Roger S Y FooGenome Institute of Singapore (W.L.W.T., C.G.A.-N., I.L., R.S.Y.F.).
Arne Hansen
Thomas EschenhagenInstitute of Experimental Pharmacology and Toxicology (A.M., G.H., M.N.H., S.D.L., T.E., J.S.), University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Justus StenzigInstitute of Experimental Pharmacology and Toxicology (A.M., G.H., M.N.H., S.D.L., T.E., J.S.), University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Universität Hamburg · DEGenome Institute of Singapore · SGNational University Heart Centre Singapore · SGGerman Centre for Cardiovascular Research · DEUniversity of Nottingham · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDNA methylation acts as a mechanism of gene transcription regulation. It has recently gained attention as a possible therapeutic target in cardiac hypertrophy and heart failure. However, its exact role in cardiomyocytes remains controversial. Thus, we knocked out the main de novo DNA methyltransferase in cardiomyocytes, DNMT3A, in human induced pluripotent stem cells. Functional consequences of DNA methylation-deficiency under control and stress conditions were then assessed in human engineered heart tissue from knockout human induced pluripotent stem cell-derived cardiomyocytes.

methods

resultsKnockout of

conclusionThe results suggest an important role of DNA methylation in the normal homeostasis of cardiomyocytes and during cardiac stress, which could make it an interesting target for cardiac therapy.

Indexed as

CardiomegalyDNA (Cytosine-5-)-MethyltransferasesDNA MethylationDNA Methyltransferase 3AEpigenomicsGene Expression RegulationHumansMyocytes, CardiacTissue EngineeringDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3ADNMT3A protein, humancardiac hypertrophyepigeneticstissue engineering

Identifiers

PMID32885664
PMCPMC7566310
OpenAlexW3083662059

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.