Galectin-3 Regulates Atrial Fibrillation Remodeling and Predicts Catheter Ablation Outcomes

著者: Yoshio Takemoto, Rafael J. Ramírez, Miki Yokokawa, Kuljeet Kaur, Daniela Ponce‐Balbuena, Mohamad Sinno, B. Cicero Willis, Hamid Ghanbari, Steven R. Ennis, Guadalupe Guerrero‐Serna, Bettina Henzi, Rakesh Latchamsetty, Roberto Ramos‐Mondragón, Hassan Musa, Raphaël P. Martins, Sandeep V. Pandit, Sami F. Noujaim, Thomas Crawford, Krit Jongnarangsin, Frank Pelosi, Frank Bogun, Aman Chugh, Omer Berenfeld, Fred Morady, Hakan Oral, José Jalife - JACC Basic to Translational Science 2016 被引用: 134

OBJECTIVES: To determine whether Gal-3 mediates sustained atrial fibrillation (AF)-induced atrial structural and electrical remodeling and contributes to AF perpetuation. BACKGROUND: Galectin-3 (Gal-3) mediates extracellular matrix remodeling in heart failure, but its role in AF progression remains unexplored. METHODS: ), we tested the effects of Gal-3 inhibition during AF progression. RESULTS: channel (Kir2.3) than saline-treated animals. Importantly, GMCT increased the probability of spontaneous AF termination, decreased AF inducibility and reduced overall AF burden. CONCLUSIONS: Inhibiting Gal-3 during AF progression might be useful as an adjuvant treatment to improve outcomes of catheter ablation for persistent AF. Gal-3 inhibition may be a potential new upstream therapy for prevention of AF progression.