Atrial fibrillation (AF) is the most common clinically significant arrhythmia. There are four fundamental pathophysiological mechanisms of AF including: electrical remodeling, structural remodeling, autonomic nervous system changes, and Ca2+ handling abnormalities. The transforming growth factor-β (TGF-β) superfamily are cytokines that have the ability to regulate numerous cell functions including proliferation, differentiation, apoptosis, epithelial-mesenchymal transition, and production of extracellular matrix. During the last decade numerous studies have demonstrated that TGF-β affects the architecture of the heart. TGF-β1 has been shown to be involved in the development and propagation of atrial fibrillation (AF). Investigators have studied TGF-β signaling in AF with the aim of discovering potential therapeutic agents. In this review we discuss the role of TGF-β in atrial fibrillation and specifically its role in atrial structural and electrical remodeling.
Keywords: Atrial fibrillation; Electrical remodeling; Fibrosis; Structural remodeling; Transforming growth factor-β.
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