Empagliflozin reduces myocardial damage and improves myocardial function after CRS-3. * Empagliflozin normalizes the mitochondrial structure in cardiomyocytes during CRS-3. * Empagliflozin attenuates cardiomyocyte mitochondrial dysfunction during CRS-3. * Empagliflozin activates FUNDC1-dependent mitophagy and preserves mitochondrial integrity in the heart during CRS-3. * Loss of FUNDC1 abolishes the cardioprotective effects of empagliflozin during CRS-3.
Conclusion: In summary, empagliflozin activated Wnt/β-catenin to stimulate FUNDC1-dependent mitochondrial quality surveillance, ultimately improving mitochondrial function and cardiac performance during CRS-3. Thus, empagliflozin could be considered for the clinical management of heart function following acute kidney injury.