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RGS4-knockout mice and pacemaker cells of the sinoatrial node (SAN)
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RGS4 loss may heighten bradyarrhythmia susceptibility in mice; leaves open its relevance to human sinus node dysfunction or AF.
RGS4 functions as a key regulator of parasympathetic signaling in the sinoatrial node, and its loss may increase susceptibility to bradyarrhythmias and atrial fibrillation.
Mighiu et al. (2012) studied this question.
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