The sodium/glucose cotransporter 2 inhibitor empagliflozin is a pharmacological chaperone of cardiac Na_v1.5 channels.

ABSTRACT: Diminished peak sodium current (I_Na) is a causative factor for slowed ventricular conduction and cardiac arrhythmias in patients with Duchenne muscular dystrophy (DMD), a devastating muscle disease triggered by dystrophin deficiency. Recently, we showed that chronic administration of the sodium/glucose cotransporter 2 (SGLT2) inhibitor empagliflozin (EMPA) restores diminished peak I_Na in ventricular cardiomyocytes from the dystrophin-deficient mdx mouse model of DMD. Here, we aimed to elucidate the underlying mechanism. Whole cell patch clamp studies revealed that 24-h incubation of dystrophic (mdx) ventricular cardiomyocytes with EMPA significantly increases peak I_Na in a concentration-dependent manner (EC₅₀ =

SUBMITTER: Sauer J 

PROVIDER: S-EPMC7618122 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature