ArticleThe Journal of cell biology2016
Postnatal telomere dysfunction induces cardiomyocyte cell-cycle arrest through p21 activation.
Article in The Journal of cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 84 citations in OpenAlex.
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- Targeting Cardiomyocyte PCNA and POLD1 Prevents Pathologic Myocardial Hypertrophy.Circulation research · 2025Article
- Systemic aging fuels heart failure: Molecular mechanisms and therapeutic avenues.ESC heart failure · 2025Review
- Nucleic acid therapeutics: Past, present, and future.Molecular therapy. Nucleic acids · 2025Review
- YAP Overcomes Mechanical Barriers to Induce Mitotic Rounding and Adult Cardiomyocyte Division.Circulation · 2025Article
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- Telomerase-Mediated Anti-Ageing Interventions.Sub-cellular biochemistry · 2024Review
- High-fat stimulation induces atrial neural remodeling by reducing NO production via the CRIF1/eNOS/P21 axi.Lipids in health and disease · 2023Article
- p53 in the Molecular Circuitry of Bone Marrow Failure Syndromes.International journal of molecular sciences · 2023Review
- Cellular polyploidy in organ homeostasis and regeneration.Protein & cell · 2023Article
- NIH SenNet Consortium to map senescent cells throughout the human lifespan to understand physiological health.Nature aging · 2022Article
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- Nucleated red blood cells participate in myocardial regeneration in the toadExperimental biology and medicine (Maywood, N.J.) · 2021Article
- Induced Cardiomyocyte Proliferation: A Promising Approach to Cure Heart Failure.International journal of molecular sciences · 2021Review
- Polyploid cardiomyocytes: implications for heart regeneration.Development (Cambridge, England) · 2021Article
- Evidence that the acetyltransferase Tip60 induces the DNA damage response and cell-cycle arrest in neonatal cardiomyocytes.Journal of molecular and cellular cardiology · 2021Article
- Cellular aging beyond cellular senescence: Markers of senescence prior to cell cycle arrest in vitro and in vivo.Aging cell · 2021Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The molecular mechanisms that drive mammalian cardiomyocytes out of the cell cycle soon after birth remain largely unknown. Here, we identify telomere dysfunction as a critical physiological signal for cardiomyocyte cell-cycle arrest. We show that telomerase activity and cardiomyocyte telomere length decrease sharply in wild-type mouse hearts after birth, resulting in cardiomyocytes with dysfunctional telomeres and anaphase bridges and positive for the cell-cycle arrest protein p21. We further show that premature telomere dysfunction pushes cardiomyocytes out of the cell cycle. Cardiomyocytes from telomerase-deficient mice with dysfunctional telomeres (G3 Terc(-/-)) show precocious development of anaphase-bridge formation, p21 up-regulation, and binucleation. In line with these findings, the cardiomyocyte proliferative response after cardiac injury was lost in G3 Terc(-/-) newborns but rescued in G3 Terc(-/-)/p21(-/-) mice. These results reveal telomere dysfunction as a crucial signal for cardiomyocyte cell-cycle arrest after birth and suggest interventions to augment the regeneration capacity of mammalian hearts.
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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.