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July 23, 2026Journal of Molecular and Cellular CardiologyOpen Access

TBX5-p.G125R mutation postnatally deregulates pacemaker cardiomyocytes in mice, demonstrating TBX5's critical role in cell maintenance.

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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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