ReviewPhysiological reviews2007
Cardiac myocyte cell cycle control in development, disease, and regeneration.
Review in Physiological reviews, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 289 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
289 citing papers in PubMed, 2 syntheses or guidelines pooled it, 564 citations in OpenAlex.
- A Meta-Analysis Approach to Gene Regulatory Network Inference Identifies Key Regulators of Cardiovascular Diseases.International journal of molecular sciences · 2024Pooled it
- Meta-analysis of Transcriptomic Data Reveals Pathophysiological Modules Involved with Atrial Fibrillation.Molecular diagnosis & therapy · 2020Pooled it
- Chronic Senolytic Treatment and/or Aerobic Exercise Reduce Senescence and Improve Myocardial Function During Aging in the Heart.Aging cell · 2026Article
- Contractility Drives Cardiomyocyte Maturation and the Response to Nanopatterns.Circulation research · 2026Article
- Signaling pathways regulating cardiac regeneration.Cell regeneration (London, England) · 2026Review
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- Article
- Gastrodin alleviates cardiomyocyte senescence by regulating autophagy through the AMPK/mTOR/4EBP1 pathway.Frontiers in pharmacology · 2026Article
- C-C motif receptor 2 is a core profibrotic factor in uremic cardiomyopathy.Disease models & mechanisms · 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
- Transcytotic transportation of size-controlled nanocarriers into dystrophic skeletal muscle leads to therapeutic outcome in mice.Nature communications · 2025Article
- Quantification of morphological, functional, and biochemical features of H9c2 rat cardiomyoblast retinoic acid differentiation.Journal of molecular and cellular cardiology plus · 2025Article
- Targeting the Hippo Pathway for Cardiac Regeneration.Physiology (Bethesda, Md.) · 2025Review
- Deciphering the Role of Different Ceramide Synthases in the Human Cardiomyocyte Hypertrophic Response.Metabolites · 2025Article
- Heart-derived endogenous stem cells.Molecular biology reports · 2025Review
- Longitudinal Multi-Organ Transcriptomic Atlas of Salt-Induced Hypertension.bioRxiv : the preprint server for biology · 2025Article
- The Role of AMPKα in the Mechanism of Development and Treatment of Heart Failure.Reviews in cardiovascular medicine · 2025Review
- Tumour initiated purinergic signalling promotes cardiomyocyte RBFOX1 degradation and cardiotoxicity from DNA damaging anticancer agents.Nature communications · 2025Article
- Immunization induces inflammation in the mouse heart during spaceflight.BMC genomics · 2025Article
- Polyphenol-Nanoengineered Monocyte Biohybrids for Targeted Cardiac Repair and Immunomodulation.Advanced healthcare materials · 2025Article
229 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
3 authors at 1 institution in 1 country.
Funding
Abstract
Cardiac myocytes rapidly proliferate during fetal life but exit the cell cycle soon after birth in mammals. Although the extent to which adult cardiac myocytes are capable of cell cycle reentry is controversial and species-specific differences may exist, it appears that for the vast majority of adult cardiac myocytes the predominant form of growth postnatally is an increase in cell size (hypertrophy) not number. Unfortunately, this limits the ability of the heart to restore function after any significant injury. Interest in novel regenerative therapies has led to the accumulation of much information on the mechanisms that regulate the rapid proliferation of cardiac myocytes in utero, their cell cycle exit in the perinatal period, and the permanent arrest (terminal differentiation) in adult myocytes. The recent identification of cardiac progenitor cells capable of giving rise to cardiac myocyte-like cells has challenged the dogma that the heart is a terminally differentiated organ and opened new prospects for cardiac regeneration. In this review, we summarize the current understanding of cardiomyocyte cell cycle control in normal development and disease. In addition, we also discuss the potential usefulness of cardiomyocyte self-renewal as well as feasibility of therapeutic manipulation of the cardiac myocyte cell cycle for cardiac regeneration.
Indexed as
Identifiers
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.