Transgenic mice overexpressing Pitx2 in the atria develop tachycardia-bradycardia syndrome.

ABSTRACT: Sinoatrial node (SAN) dysfunction often accompanies supraventricular tachyarrhythmias such as atrial fibrillation (AF), which is referred to as tachycardia-bradycardia syndrome (TBS). Although there have been many studies on electrical remodeling in TBS, the regulatory mechanisms that cause electrical remodeling in the SAN and atrial muscles by chronic bradycardia or tachycardia have not yet been fully investigated. Here we hypothesized Pitx2c, a transcription factor that played a central role in the late aspects of left-right asymmetric morphogenesis, regulated an interrelationship between the SAN and the atrial muscles and was involved in TBS-like pathology. To test this hypothesis, we generated transgenic mice overexpressing Pitx2c specifically in the atria (OE mice). Although Pitx2c is

SUBMITTER: Baba S 

PROVIDER: S-EPMC12410714 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature