Evidence map›Paper›PMID 34723970›Full record

ArticlePLoS genetics2021

Histone deacetylase 1 controls cardiomyocyte proliferation during embryonic heart development and cardiac regeneration in zebrafish.

Anja Bühler, Bernd M Gahr, Deung-Dae Park, Alberto Bertozzi, Alena Boos, Mohankrishna Dalvoy, Alexander Pott, Franz Oswald, Rhett A Kovall, Bernhard Kühn and 3 more

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

11 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
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

13 authors at 3 institutions in 2 countries.

Anja BühlerMolecular Cardiology, Department of Internal Medicine II, University of Ulm, Ulm, Germany.ORCID 0000-0003-2927-2379
Bernd M GahrMolecular Cardiology, Department of Internal Medicine II, University of Ulm, Ulm, Germany.ORCID 0000-0002-5755-6603
Deung-Dae ParkMolecular Cardiology, Department of Internal Medicine II, University of Ulm, Ulm, Germany.ORCID 0000-0001-6265-4964
Alberto BertozziInstitute of Biochemistry and Molecular Biology, University of Ulm, Ulm, Germany.ORCID 0000-0003-3091-1481
Alena BoosMolecular Cardiology, Department of Internal Medicine II, University of Ulm, Ulm, Germany.
Mohankrishna DalvoyInstitute of Biochemistry and Molecular Biology, University of Ulm, Ulm, Germany.ORCID 0000-0003-4430-4893
Alexander PottMolecular Cardiology, Department of Internal Medicine II, University of Ulm, Ulm, Germany.
Franz OswaldDepartment of Internal Medicine I, University of Ulm, Ulm, Germany.
Rhett A KovallDepartment of Molecular Genetics, Biochemistry and Microbiology, University of Cincinnati College of Medicine, Cincinnati, Ohio, United States of America.ORCID 0000-0003-0520-1613
Bernhard KühnDepartment of Pediatrics, University of Pittsburgh, and Richard King Mellon Institute for Pediatric Research and Division of Pediatric Cardiology, Children's Hospital of Pittsburgh of UPMC, Pittsburgh, Pennsylvania, United States of America.ORCID 0000-0002-1855-7072
Gilbert WeidingerInstitute of Biochemistry and Molecular Biology, University of Ulm, Ulm, Germany.ORCID 0000-0003-3599-6760
Wolfgang RottbauerDepartment of Internal Medicine II, University of Ulm, Ulm, Germany.ORCID 0000-0003-4725-6217
Steffen JustMolecular Cardiology, Department of Internal Medicine II, University of Ulm, Ulm, Germany.ORCID 0000-0001-7396-1281
Universität Ulm · DEUniversity of Cincinnati Medical Center · USUniversity of Pittsburgh · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In contrast to mammals, the zebrafish maintains its cardiomyocyte proliferation capacity throughout adulthood. However, neither the molecular mechanisms that orchestrate the proliferation of cardiomyocytes during developmental heart growth nor in the context of regeneration in the adult are sufficiently defined yet. We identified in a forward genetic N-ethyl-N-nitrosourea (ENU) mutagenesis screen the recessive, embryonic-lethal zebrafish mutant baldrian (bal), which shows severely impaired developmental heart growth due to diminished cardiomyocyte proliferation. By positional cloning, we identified a missense mutation in the zebrafish histone deacetylase 1 (hdac1) gene leading to severe protein instability and the loss of Hdac1 function in vivo. Hdac1 inhibition significantly reduces cardiomyocyte proliferation, indicating a role of Hdac1 during developmental heart growth in zebrafish. To evaluate whether developmental and regenerative Hdac1-associated mechanisms of cardiomyocyte proliferation are conserved, we analyzed regenerative cardiomyocyte proliferation after Hdac1 inhibition at the wound border zone in cryoinjured adult zebrafish hearts and we found that Hdac1 is also essential to orchestrate regenerative cardiomyocyte proliferation in the adult vertebrate heart. In summary, our findings suggest an important and conserved role of Histone deacetylase 1 (Hdac1) in developmental and adult regenerative cardiomyocyte proliferation in the vertebrate heart.

Indexed as

AnimalsCell ProliferationHeartHistone Deacetylase 1Myocytes, CardiacRegenerationZebrafishZebrafish ProteinsHDAC1 protein, zebrafishHistone Deacetylase 1Zebrafish Proteins

Identifiers

PMID34723970
PMCPMC8584950
OpenAlexW3208064339

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.