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Updated: Mar 20, 2026

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Postnatal telomere dysfunction induces cardiomyocyte cell-cycle arrest through p21 activation

Esther Aix1, Óscar Gutiérrez-Gutiérrez1, Carlota Sánchez-Ferrer1

  • 1Centro Nacional de Investigaciones Cardiovasculares Carlos III, 28029 Madrid, Spain.

The Journal of Cell Biology
|June 1, 2016
PubMed

Insights

Telomere dysfunction signals mammalian cardiomyocytes to exit the cell cycle after birth. Restoring cardiomyocyte proliferation in telomere-dysfunctional mice by inhibiting p21 suggests potential heart regeneration strategies.

Area of Science:

  • Cardiovascular Biology
  • Cellular Aging
  • Molecular Cardiology

Background:

  • Mammalian cardiomyocyte cell-cycle exit post-birth is poorly understood.
  • Identifying triggers for cardiomyocyte proliferation arrest is crucial for cardiac repair.

Purpose of the Study:

  • To investigate the role of telomere dysfunction in cardiomyocyte cell-cycle arrest.
  • To explore therapeutic targets for enhancing cardiac regeneration.

Main Methods:

  • Assessed telomerase activity and telomere length in wild-type and telomerase-deficient (G3 Terc(-/-)) mouse hearts.
  • Examined cell-cycle markers (p21) and telomere integrity.
  • Investigated cardiomyocyte proliferation after cardiac injury in G3 Terc(-/-) and G3 Terc(-/-)/p21(-/-) mice.

Main Results:

  • Telomere length and telomerase activity decrease post-birth in wild-type mice, leading to telomere dysfunction and cell-cycle arrest.
  • Premature telomere dysfunction in G3 Terc(-/-) mice caused precocious cell-cycle arrest, p21 up-regulation, and binucleation.
  • Loss of cardiomyocyte proliferation after injury in G3 Terc(-/-) newborns was rescued in G3 Terc(-/-)/p21(-/-) mice.

Conclusions:

  • Telomere dysfunction is a critical signal for cardiomyocyte cell-cycle arrest after birth.
  • Targeting p21 may offer a strategy to enhance mammalian heart regeneration.

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