PARP1 and atrial fibrillation: The findings reveal that tachypacing (TP)-induced cardiomyocyte dysfunction is a consequence of DNA damage-modulated PARP1 activation, which leads to depletion of nicotinamide adenine dinucleotide (NAD+) and further oxidative stress and DNA damage and implicate PARP1 as a possible therapeutic target that may preserve cardiomyocyte function in AF.