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July 23, 2026Journal of Molecular and Cellular CardiologyOpen Access

TBX5-p.G125R postnatally deregulates pacemaker cardiomyocyte state and function

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Key result

The TBX5-p.G125R mutation postnatally deregulates pacemaker cardiomyocyte state and function in mice, demonstrating the critical role of TBX5 in maintaining these cells.

Authors

LMLieve E. van der MaarelOMOtto J. MullenersLSLaura H.F. Stoop

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Overview

Offers preclinical insight into TBX5-dependent pacemaker regulation; leaves open translation to human sinus node disease.

Key Points

  • The research aims to explore how the TBX5-p.G125R mutation affects cardiomyocyte function postnatally.
  • Examine the effects of TBX5-p.G125R mutation in mice.
  • Assess pacemaker cardiomyocyte state and function.
  • The TBX5-p.G125R mutation significantly disrupts pacemaker cardiomyocyte function.
  • Maintaining TBX5 levels is crucial for proper cardiomyocyte state.

Cite This Study

Maarel et al. (2026) studied this question. The TBX5-p.G125R mutation postnatally deregulates pacemaker cardiomyocyte state and function in mice, demonstrating the critical role of TBX5 in maintaining these cells.

synapsesocial.com/papers/6a61aea0faa9903c51169e4ahttps://doi.org/10.1016/j.yjmcc.2026.07.012
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Also Consider

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

  1. 1Abstract Thu099: Single-Cell RNA-seq Analysis Reveals a Two-Step Mechanism for TBX18-Mediated Reprogramming of Ventricular Myocytes into Pacemaker Cells2025
  2. 2Reduced TBX5 dosage undermines developmental control of atrial cardiomyocyte identity in a model of human atrial disease2025 · 1 citations
  3. 3AAV-mediated long-term TBX18 expression causes cardiac fibrosis and fails to induce pacemaker activity in rodents2026
  4. 4TBX5 and CHD4 Coordinately Activate Atrial Cardiomyocyte Genes to Maintain Cardiac Rhythm Homeostasis.2025
  5. 5Abstract NBT102: RBX1 Is an Indispensable, Dosage-Sensitive Regulator of Perinatal Heart Development2025