Evidence map›Paper›PMID 33500391›Full record

ReviewSignal transduction and targeted therapy2021

Regulation of cardiomyocyte fate plasticity: a key strategy for cardiac regeneration.

Rui Gong, Zuke Jiang, Naufal Zagidullin, Tianyi Liu, Benzhi Cai

Abstract readReview
In one paragraph

Review in Signal transduction and targeted therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing 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

47 citing papers in PubMed.

  1. Biologics for cardiovascular diseases: from bench to bedside.Signal transduction and targeted therapy · 2026
    Review
  2. Article
  3. Review
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  5. CD160Cellular & molecular immunology · 2026
    Article
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  9. Article
  10. The role of mechanosignaling in the control of myocardial mass.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  11. Article
  12. Gut microbiota and atrial cardiomyopathy.Frontiers in cardiovascular medicine · 2025
    Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
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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

5 authors.

Rui Gong *Department of Pharmacy at the Second Affiliated Hospital, and Department of Pharmacology (The Key Laboratory of Cardiovascular Research, Ministry of Education) at College of Pharmacy, Harbin Medical University, 150086, Harbin, China.
Zuke Jiang *Department of Pharmacy at the Second Affiliated Hospital, and Department of Pharmacology (The Key Laboratory of Cardiovascular Research, Ministry of Education) at College of Pharmacy, Harbin Medical University, 150086, Harbin, China.
Naufal ZagidullinDepartment of Internal Diseases, Bashkir State Medical University, Ufa, 450008, Russia.
Tianyi LiuCollege of Pharmacy, University of Cincinnati, Cincinnati, OH, USA.
Benzhi CaiDepartment of Pharmacy at the Second Affiliated Hospital, and Department of Pharmacology (The Key Laboratory of Cardiovascular Research, Ministry of Education) at College of Pharmacy, Harbin Medical University, 150086, Harbin, China. caibz@ems.hrbmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

With the high morbidity and mortality rates, cardiovascular diseases have become one of the most concerning diseases worldwide. The heart of adult mammals can hardly regenerate naturally after injury because adult cardiomyocytes have already exited the cell cycle, which subseqently triggers cardiac remodeling and heart failure. Although a series of pharmacological treatments and surgical methods have been utilized to improve heart functions, they cannot replenish the massive loss of beating cardiomyocytes after injury. Here, we summarize the latest research progress in cardiac regeneration and heart repair through altering cardiomyocyte fate plasticity, which is emerging as an effective strategy to compensate for the loss of functional cardiomyocytes and improve the impaired heart functions. First, residual cardiomyocytes in damaged hearts re-enter the cell cycle to acquire the proliferative capacity by the modifications of cell cycle-related genes or regulation of growth-related signals. Additionally, non-cardiomyocytes such as cardiac fibroblasts, were shown to be reprogrammed into cardiomyocytes and thus favor the repair of damaged hearts. Moreover, pluripotent stem cells have been shown to transform into cardiomyocytes to promote heart healing after myocardial infarction (MI). Furthermore, in vitro and in vivo studies demonstrated that environmental oxygen, energy metabolism, extracellular factors, nerves, non-coding RNAs, etc. play the key regulatory functions in cardiac regeneration. These findings provide the theoretical basis of targeting cellular fate plasticity to induce cardiomyocyte proliferation or formation, and also provide the clues for stimulating heart repair after injury.

Indexed as

AnimalsCardiovascular DiseasesCell CycleCell LineageCell PlasticityHeartHumansMyocytes, CardiacRegeneration

Identifiers

PMID33500391
PMCPMC7838318

What OpenQuestion holds

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LicenceCC BY
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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.