Beyond Glycemic Control: Ipragliflozin Mitigates Atrial Fibrillation and Myocardial Remodeling through Mitochondrial Protection

This study systematically investigated the effects and mechanisms of the hypoglycemic drug Ipragliflozin in treating atrial fibrillation unrelated to diabetes through animal and cellular experiments. The research found that Ipragliflozin significantly alleviated the occurrence of atrial fibrillation independently of its blood glucose-lowering effect. The core mechanism lies in protecting myocardial mitochondria: improving mitochondrial structure and function, enhancing mitochondrial biogenesis, reducing oxidative stress, and thereby inhibiting cardiomyocyte apoptosis, inflammation, and fibrosis. These findings suggest that SGLT2 inhibitors like Ipragliflozin may exert antiarrhythmic effects through a "direct cardioprotective" mitochondrial protection pathway, providing new theoretical evidence for their potential as therapeutic agents for atrial fibrillation.