TBX5-p.G125R postnatally deregulates pacemaker cardiomyocyte state and function.
It is concluded that alterations driven by TBX5-p.G125R in the transcriptional state of the postnatal sinus node contribute to sinus node dysfunction and atrial arrhythmias in adult Tbx5+/G125R mice, emphasizing the critical role of TBX5 in maintaining pacemaker cardiomyocyte state and function.