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Atrial fibrillation (AF) is a growing public health problem without adequate therapies. Angiotensin II and reactive oxygen species are validated risk factors for AF in patients, but the molecular pathways connecting reactive oxygen species and AF are unknown. The Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) has recently emerged as a reactive oxygen species-activated proarrhythmic signal, so we hypothesized that oxidized CaMKIIδ could contribute to AF.

Oxidized Ca 2+ /Calmodulin-Dependent Protein Kinase II Triggers Atrial Fibrillation

Oxidized Ca ²⁺ /Calmodulin-Dependent Protein Kinase II Triggers Atrial Fibrillation