ReviewJournal of cellular and molecular medicine2008
Features of cardiomyocyte proliferation and its potential for cardiac regeneration.
Review in Journal of cellular and molecular medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 2 of them syntheses that pooled 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.
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.
Who cites it
65 citing papers in PubMed, 2 syntheses or guidelines pooled it, 124 citations in OpenAlex.
- RNA-Binding Protein Signature in Proliferative Cardiomyocytes: A Cross-Species Meta-Analysis from Mouse, Pig, and Human Transcriptomic Profiling Data.Biomolecules · 2025Pooled it
- Pooled it
- Mesenchymal Stromal Cells Improve Postoperative Cardiac Dysmaturation in a Juvenile Porcine Model.Journal of the American Heart Association · 2026Article
- Placental insufficiency disrupts cardiomyocyte ploidy and cell cycle fate in growth-restricted fetal sheep.American journal of physiology. Regulatory, integrative and comparative physiology · 2026Article
- Review
- Article
- Exploring the Function of Epicardial Cells Beyond the Surface.Circulation research · 2024Review
- Epigenetic Regulation of Mammalian Cardiomyocyte Development.Epigenomes · 2024Review
- Bioreactor Design for Culturing Vascularized Engineered Tissue in Flow Conditions.Tissue engineering. Part A · 2024Article
- Integrated small RNA, mRNA and protein omics reveal a miRNA network orchestrating metabolic maturation of the developing human heart.BMC genomics · 2023Article
- Direct cardiac reprogramming: A new technology for cardiac repair.Journal of molecular and cellular cardiology · 2023Review
- Research Progress of Exosomal Non-Coding RNAs in Cardiac Remodeling.International journal of medical sciences · 2023Review
- Modeling the human heart ex vivo-current possibilities and strive for future applications.Journal of tissue engineering and regenerative medicine · 2022Review
- Exosomes in cardiovascular diseases: a blessing or a sin for the mankind.Molecular and cellular biochemistry · 2022Review
- Article
- CHIR99021 Promotes hiPSC-Derived Cardiomyocyte Proliferation in Engineered 3D Microtissues.Advanced healthcare materials · 2021Article
- Alternative Splicing of Pericentrin Contributes to Cell Cycle Control in Cardiomyocytes.Journal of cardiovascular development and disease · 2021Article
- Apex Resection in Zebrafish (International journal of molecular sciences · 2021Article
- Cardiomyocyte nuclearity and ploidy: when is double trouble?Journal of muscle research and cell motility · 2020Article
- Isolation, Transfection, and Long-Term Culture of Adult Mouse and Rat Cardiomyocytes.Journal of visualized experiments : JoVE · 2020Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The human heart does not regenerate. Instead, following injury, human hearts scar. The loss of contractile tissue contributes significantly to morbidity and mortality. In contrast to humans, zebrafish and newts faithfully regenerate their hearts. Interestingly, regeneration is in both cases based on cardiomyocyte proliferation. In addition, mammalian cardiomyocytes proliferate during foetal development. Their proliferation reaches its maximum around chamber formation, stops shortly after birth, and subsequent heart growth is mostly achieved by an increase in cardiomyocyte size (hypertrophy). The underlying mechanisms that regulate cell cycle arrest and the switch from proliferation to hypertrophy are unclear. In this review, we highlight features of dividing cardiomyocytes, summarize the attempts to induce mammalian cardiomyocyte proliferation, critically discuss methods commonly used for its detection, and explore the potential and problems of inducing cardiomyocyte proliferation to improve function in diseased hearts.
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What OpenQuestion holds
Registered trials
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.