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Atrial fibrillation (AF) is the most common arrhythmia in humans. It affects 5% of the population over the age of 65 years and is projected to rise as the population ages. Experimental data from animal models of AF shows that AF is associated with progressive structural and electrical remodeling of the atria. Atrial fibrosis alters atrial electrical conduction and excitability and provides a substrate for AF maintenance. However, whether fibrosis is causally related to AF or an epiphenomenon, and the precise mechanisms underlying atrial fibrosis remain unclear. A variety of signaling systems involving angiotensin II and related mediators, are centrally involved in atrial fibrosis. This article will review the role that atrial fibrosis plays in AF, the mechanisms of atrial fibrosis, and emerging therapeutic approaches to AF aimed at attenuating atrial fibrosis.