To determine the chronic in vivo effects of empagliflozin on cardiomyocyte electrophysiology, excitation-contraction coupling (ECC), and transcriptome profile in a mouse model of HFpEF, highlighting its potential therapeutic implications.
Approach:
Key Findings:
Empagliflozin treatment improved diastolic function and reduced proarrhythmogenic action potential changes, with specific metrics indicating the degree of improvement.
Chronic treatment restored cardiomyocyte electrophysiology and ECC mechanisms, suggesting a reversal of pathological changes.
Empagliflozin modified gene expression profiles in the heart, with implications for understanding its mechanism of action.
Interpretation:
Empagliflozin has lasting effects on cardiac function and gene expression in HFpEF, indicating potential therapeutic benefits beyond glycemic control, warranting further investigation in clinical settings.
Limitations:
Study conducted in a specific mouse model, which may not fully represent human HFpEF, necessitating caution in extrapolation.
Results may not be generalizable to other populations or treatment regimens, highlighting the need for diverse clinical trials.
Conclusion:
Empagliflozin demonstrates significant improvements in cardiac function and gene expression in a mouse model of HFpEF, suggesting its potential as a therapeutic agent in heart failure management.
by Juliana Mira Hernandez, Logan R. J. Bailey, Victoria R. Salemme, Christopher Y. Ko, Erin Y. Shen, Megan Ngim, Duong T. Hoang, Melissa Corea, Julie Bossuyt, Jennifer M. Davis, Donald M. Bers, Bence Hegyi
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