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August 19, 2025Open Access

Reduced TBX5 dosage undermines developmental control of atrial cardiomyocyte identity in a model of human atrial disease

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Authors

IKIrfan S. KathiriyaKRKavitha S. RaoACAlexander P. Clark

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Overview

Directed differentiation shows TBX5 affects cardiomyocyte identity in atrial diseases, suggesting implications for AF and ASDs.

Key Points

  • Reduced dosage of tbx5 caused a significant disruption in atrial cardiomyocyte identity and function.
  • Complete tbx5 loss nearly eliminated atrial cardiomyocytes, while increasing other cell types present.
  • Investigation utilized human induced pluripotent stem cells to probe gene regulatory networks involved in atrial and ventricular cardiomyocyte identity.
  • These findings may highlight a genetic link between atrial diseases and impaired gene regulation critical for proper atrial cardiomyocyte identity.

Cite This Study

Kathiriya et al. (2025) studied this question.

synapsesocial.com/papers/68af751a7567bf4f94fee3e1https://doi.org/10.1101/2025.08.16.669546
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1TBX5 and CHD4 Coordinately Activate Atrial Cardiomyocyte Genes to Maintain Cardiac Rhythm Homeostasis.2025
  2. 2Novel TBX20 Variations Susceptible to Sporadic Atrial Fibrillation2026
  3. 3AAV-mediated long-term TBX18 expression causes cardiac fibrosis and fails to induce pacemaker activity in rodents2026
  4. 4TBX5-p.G125R postnatally deregulates pacemaker cardiomyocyte state and function2026
  5. 5Discovery of SOX5 as a New Causative Gene for Atrial Fibrillation2025