Evidence map›Paper›PMID 26657817›Full record

ArticleScientific reports2015

Epigenomic Reprogramming of Adult Cardiomyocyte-Derived Cardiac Progenitor Cells.

Yiqiang Zhang, Jiang F Zhong, Hongyu Qiu, W Robb MacLellan, Eduardo Marbán, Charles Wang

Erratum issuedAbstract read
In one paragraph

Article in Scientific reports, 2015. 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 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
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

19 citing papers in PubMed.

  1. Article
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  5. Article
  6. Article
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  8. Review
  9. Article
  10. Article
  11. Epigenomes in Cardiovascular Disease.Circulation research · 2018
    Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors.

Yiqiang ZhangDivision of Cardiology, Department of Medicine, and Center for Cardiovascular Biology, and Institute for Stem Cell and Regenerative Medicine, University of Washington, Seattle, WA 98109, USA.
Jiang F ZhongOstrow School of Dentistry and Department of Pediatrics, School of Medicine, University of Southern California, Los Angeles, CA 90089, USA.
Hongyu QiuDepartment of Basic Sciences, School of Medicine, Loma Linda University, Loma Linda, CA 92350, USA.
W Robb MacLellanDivision of Cardiology, Department of Medicine, and Center for Cardiovascular Biology, and Institute for Stem Cell and Regenerative Medicine, University of Washington, Seattle, WA 98109, USA.
Eduardo MarbánThe Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, 90048, USA.
Charles WangCenter for Genomics &Department of Basic Sciences, School of Medicine, Loma Linda University, Loma Linda, CA, 92350, USA.

Funding

Intrinsic Stiffness of Aortic Vascular Smooth Muscle Cell in the Development of HypertensionR01HL115195 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI QIU, HONGYU · 2013 to 2022
$5.1M
Electrophysiology and Cell Biology of Cardiac Stem CellsR01HL083109 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI MARBAN, EDUARDO · 2006 to 2014
$3.6M
NHLBI NIH HHS R01 HL083109NHLBI NIH HHS R01HL083109NHLBI NIH HHS R01 HL115195
6 · The paper itself

Abstract

It has been believed that mammalian adult cardiomyocytes (ACMs) are terminally-differentiated and are unable to proliferate. Recently, using a bi-transgenic ACM fate mapping mouse model and an in vitro culture system, we demonstrated that adult mouse cardiomyocytes were able to dedifferentiate into cardiac progenitor-like cells (CPCs). However, little is known about the molecular basis of their intrinsic cellular plasticity. Here we integrate single-cell transcriptome and whole-genome DNA methylation analyses to unravel the molecular mechanisms underlying the dedifferentiation and cell cycle reentry of mouse ACMs. Compared to parental cardiomyocytes, dedifferentiated mouse cardiomyocyte-derived CPCs (mCPCs) display epigenomic reprogramming with many differentially-methylated regions, both hypermethylated and hypomethylated, across the entire genome. Correlated well with the methylome, our transcriptomic data showed that the genes encoding cardiac structure and function proteins are remarkably down-regulated in mCPCs, while those for cell cycle, proliferation, and stemness are significantly up-regulated. In addition, implantation of mCPCs into infarcted mouse myocardium improves cardiac function with augmented left ventricular ejection fraction. Our study demonstrates that the cellular plasticity of mammalian cardiomyocytes is the result of a well-orchestrated epigenomic reprogramming and a subsequent global transcriptomic alteration.

Indexed as

Cellular ReprogrammingEpigenesis, GeneticEpigenomicsAnimalsCell DedifferentiationCellular Reprogramming TechniquesCluster AnalysisDNA MethylationGene Expression ProfilingInduced Pluripotent Stem CellsMiceModels, BiologicalMyoblasts, CardiacMyocardiumMyocytes, CardiacReproducibility of Results

Identifiers

PMID26657817
PMCPMC4677315

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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.