Atrial fibrillation (AF) is the most common clinically encountered abnormal heart beat. It is associated with an increased risk of stroke and symptoms of heart failure. Current therapies are directed toward controlling the rate of ventricular activation and preventing strokes through anticoagulation. Attempts at suppressing the arrhythmia are often ineffective, in part because the underlying pathogenesis is poorly understood. Recently, structural and electrical remodeling has been shown to occur during AF. These changes involve alterations in gene regulation and help perpetuate the arrhythmia. Some signals for remodeling are have been identified. Moreover, AF is associated with oxidative stress, and this redox imbalance may contribute to the altered gene regulation. One likely mediator of this change in transcriptional regulation is the redox sensitive transcription factor, nuclear factor-κB (NF-κB). Recently, NF-κB has been shown to downregulate transcription of the cardiac sodium channel in response to oxidative stress. NF-κB may contribute to the regulation of other ion channels, transcription factors, or splicing factors altered in AF and may represent a therapeutic target in AF management.
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