Evidence map›Paper›PMID 30189626›Full record

ReviewInternational journal of molecular sciences2018

Direct Cardiac Reprogramming: A Novel Approach for Heart Regeneration.

Hidenori Tani, Taketaro Sadahiro, Masaki Ieda

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
–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

23 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. The Role of MEF2 in Scar Formation and Angiogenesis.Journal of cosmetic dermatology · 2026
    Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Direct Reprogramming of Cardiac Fibroblasts to Repair the Injured Heart.Journal of cardiovascular development and disease · 2021
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. The Roles of Noncardiomyocytes in Cardiac Remodeling.International journal of biological sciences · 2020
    Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. 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

3 authors.

Hidenori TaniDepartment of Cardiology, Keio University School of Medicine, Tokyo 160-8582, Japan. ta.hidenori@gmail.com.ORCID 0000-0002-5042-6187
Taketaro SadahiroDepartment of Cardiology, Faculty of Medicine, University of Tsukuba, 1-1-1, Tennoudai, Tsukuba City, Ibaraki 305-8575, Japan. taket0901@hotmail.co.jp.
Masaki IedaDepartment of Cardiology, Faculty of Medicine, University of Tsukuba, 1-1-1, Tennoudai, Tsukuba City, Ibaraki 305-8575, Japan. mieda@md.tsukuba.ac.jp.ORCID 0000-0003-4724-3299

Funding

Japan Agency for Medical Research and Development the Advanced Research & Development Programs for Medical Innovation solo-type
6 · The paper itself

Abstract

Cardiac diseases are among the most common causes of death globally. Cardiac muscle has limited proliferative capacity, and regenerative therapies are highly in demand as a new treatment strategy. Although pluripotent reprogramming has been developed, it has obstacles, such as a potential risk of tumor formation, poor survival of the transplanted cells, and high cost. We previously reported that fibroblasts can be directly reprogrammed to cardiomyocytes by overexpressing a combination of three cardiac-specific transcription factors (Gata4, Mef2c, Tbx5 (together, GMT)). We and other groups have promoted cardiac reprogramming by the addition of certain miRNAs, cytokines, and epigenetic factors, and unraveled new molecular mechanisms of cardiac reprogramming. More recently, we discovered that Sendai virus (SeV) vector expressing GMT could efficiently and rapidly reprogram fibroblasts into integration-free cardiomyocytes in vitro via robust transgene expression. Gene delivery of SeV-GMT also improves cardiac function and reduces fibrosis after myocardial infarction in mice. Through direct cardiac reprogramming, new cardiomyocytes can be generated and scar tissue reduced to restore cardiac function, and, thus, direct cardiac reprogramming may serve as a powerful strategy for cardiac regeneration. Here, we provide an overview of the previous reports and current challenges in this field.

Indexed as

Cellular ReprogrammingRegenerationAnimalsCell DifferentiationEpigenesis, GeneticFibroblastsGATA4 Transcription FactorGene Expression RegulationHeartHumansMEF2 Transcription FactorsMyocytes, CardiacT-Box Domain ProteinsGATA4 Transcription FactorMEF2C protein, humanMEF2 Transcription FactorsT-Box Domain ProteinsT-box transcription factor 5cardiac regenerationcardiomyocytesdirect reprogrammingfibroblastsgene therapy

Identifiers

PMID30189626
PMCPMC6165160

What OpenQuestion holds

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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.