Atrial fibrillation (AF) is a common arrhythmia with serious clinical sequelae, yet little is known about its genetic origins. Recently, the untranscribed 98% of the human genome has been increasingly implicated in important processes such as cardiac organogenesis, physiology, and pathophysiology. Specifically, long noncoding RNAs (lncRNAs) have been shown to interact with the transcriptome in various ways that alter gene expression. Previously, multiple lncRNAs have been identified in disease processes such as heart failure, coronary artery disease, and diabetes. Multiple studies now show lncRNAs are involved in each fundamental mechanism leading to the development of AF, including structural remodeling, electrical remodeling, renin angiotensin system effects, and calcium handling abnormalities. The altered expression of lncRNAs offers genetic targets for the diagnosis and treatment of AF. This article discusses the role of lncRNAs in AF and its pathogenesis.
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