Abstract
There is growing evidence that oxidative stress is involved in the pathogenesis of atrial fibrillation. Many known triggers of oxidative stress, such as age, diabetes, smoking, inflammation, and renin angiotensin system activation are linked with an increased risk of the arrhythmia. Blockers of angiotensin II signaling and other drugs with anti-oxidant properties can reduce the incidence of atrial fibrillation. Now, studies in animal models and human tissue have shown directly that atrial fibrillation is associated with increased atrial oxidative stress. We review the evidence for a role of oxidative stress in causing atrial fibrillation and propose a unifying hypothesis that multiple triggers elicit oxidative stress which acts to enhance the risk of atrial fibrillation through ion channel dysregulation.
Keywords: Transcriptional regulation, superoxide, nitric oxide, ion channels, angiotensin II
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