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