How transforming growth factor contributes to atrial fibrillation?
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Updated: Nov 26, 2025

Optimization of Transesophageal Atrial Pacing to Assess Atrial Fibrillation Susceptibility in Mice
Published on: June 29, 2022
Savalan Babapoor-Farrokhran1, Roozbeh Tarighati Rasekhi2, Deanna Gill3
1Department of Medicine, Division of Cardiology, Einstein Medical Center, Philadelphia, PA 19141, USA.
Abstract:
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.
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