Evidence map›Paper›PMID 37315521›Full record

ArticleStem cell reports2023

MEF2C/p300-mediated epigenetic remodeling promotes the maturation of induced cardiomyocytes.

Hidenori Kojima, Taketaro Sadahiro, Naoto Muraoka, Hiroyuki Yamakawa, Hisayuki Hashimoto, Ryota Ishii, Masahiko Gosho, Yuto Abe, Yu Yamada, Koji Nakano and 9 more

Open access · goldAbstract read
In one paragraph

Article in Stem cell reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Heart Regeneration for Clinical Application.Internal medicine (Tokyo, Japan) · 2026
    Review
  6. FAPNature communications · 2025
    Article
  7. Article
  8. Cell reprogramming: methods, mechanisms and applications.Cell regeneration (London, England) · 2025
    Review
  9. Review
  10. Epigenetic landscape revealsFrontiers in nutrition · 2025
    Article
  11. Review
  12. Article
  13. 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

19 authors at 5 institutions in 2 countries.

Hidenori KojimaDepartment of Cardiology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
Taketaro SadahiroDepartment of Cardiology, Faculty of Medicine, University of Tsukuba, 1-1-1 Tennoudai, Tsukuba City, Ibaraki 305-8575, Japan.
Naoto MuraokaDepartment of Cardiology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
Hiroyuki YamakawaDepartment of Cardiology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
Hisayuki HashimotoDepartment of Cardiology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
Ryota IshiiDepartment of Biostatistics, Faculty of Medicine, University of Tsukuba, 1-1-1 Tennoudai, Tsukuba City, Ibaraki 305-8575, Japan.
Masahiko GoshoDepartment of Biostatistics, Faculty of Medicine, University of Tsukuba, 1-1-1 Tennoudai, Tsukuba City, Ibaraki 305-8575, Japan.
Yuto AbeDepartment of Cardiology, Faculty of Medicine, University of Tsukuba, 1-1-1 Tennoudai, Tsukuba City, Ibaraki 305-8575, Japan.
Yu YamadaDepartment of Cardiology, Faculty of Medicine, University of Tsukuba, 1-1-1 Tennoudai, Tsukuba City, Ibaraki 305-8575, Japan.
Koji NakanoDepartment of Cardiology, Faculty of Medicine, University of Tsukuba, 1-1-1 Tennoudai, Tsukuba City, Ibaraki 305-8575, Japan.
Seiichiro HondaDepartment of Cardiology, Faculty of Medicine, University of Tsukuba, 1-1-1 Tennoudai, Tsukuba City, Ibaraki 305-8575, Japan.
Ryo FujitaDepartment of Cardiology, Faculty of Medicine, University of Tsukuba, 1-1-1 Tennoudai, Tsukuba City, Ibaraki 305-8575, Japan.
Tatsuya AkiyamaDepartment of Cardiology, Faculty of Medicine, University of Tsukuba, 1-1-1 Tennoudai, Tsukuba City, Ibaraki 305-8575, Japan.
Yoichi SunagawaDivison of Molecular Medicine, School of Pharmaceutical Science, University of Shizuoka, Shizuoka 422-8526, Japan.
Tatsuya MorimotoDivison of Molecular Medicine, School of Pharmaceutical Science, University of Shizuoka, Shizuoka 422-8526, Japan.
Toshifumi TsukaharaArea of Bioscience and Biotechnology, Japan Advanced Institute of Science and Technology, 1-1 Asahidai, Nomi City, Ishikawa 923-1292, Japan.
Hiroyuki HiraiStanley Manne Children's Research Institute, Ann & Robert H. Lurie Children's Hospital of Chicago, Department of Pediatrics, Division of Critical Care, Northwestern University Feinberg School of Medicine, 303 E. Superior Street, Chicago, IL 60611, USA.
Keiichi FukudaDepartment of Cardiology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
Masaki IedaDepartment of Cardiology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan; Department of Cardiology, Faculty of Medicine, University of Tsukuba, 1-1-1 Tennoudai, Tsukuba City, Ibaraki 305-8575, Japan. Electronic address: mieda@md.tsukuba.ac.jp.
University of Tsukuba · JPKeio University Hospital · JPUniversity of Shizuoka · JPJapan Advanced Institute of Science and Technology · JPNorthwestern University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac transcription factors (TFs) directly reprogram fibroblasts into induced cardiomyocytes (iCMs), where MEF2C acts as a pioneer factor with GATA4 and TBX5 (GT). However, the generation of functional and mature iCMs is inefficient, and the molecular mechanisms underlying this process remain largely unknown. Here, we found that the overexpression of transcriptionally activated MEF2C via fusion of the powerful MYOD transactivation domain combined with GT increased the generation of beating iCMs by 30-fold. Activated MEF2C with GT generated iCMs that were transcriptionally, structurally, and functionally more mature than those generated by native MEF2C with GT. Mechanistically, activated MEF2C recruited p300 and multiple cardiogenic TFs to cardiac loci to induce chromatin remodeling. In contrast, p300 inhibition suppressed cardiac gene expression, inhibited iCM maturation, and decreased the beating iCM numbers. Splicing isoforms of MEF2C with similar transcriptional activities did not promote functional iCM generation. Thus, MEF2C/p300-mediated epigenetic remodeling promotes iCM maturation.

Indexed as

Chromatin Assembly and DisassemblyMEF2 Transcription FactorsMyocytes, Cardiacp300-CBP Transcription FactorsEpigenesis, GeneticEpigenomicsFibroblastsMEF2 Transcription Factorsp300-CBP Transcription Factorscardiac reprogrammingcardiomyocyteepigeneticsmaturationMEF2Cp300

Identifiers

PMID37315521
PMCPMC10277823
OpenAlexW4380629897

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.