In summary, the SGLT2 inhibitor empagliflozin ameliorates myocardial fibrosis partly through inhibition of collagen formation and deposition via the classical TGF-β/Smad pathway and decreases oxidative stress via promoting Nrf2 translocation to the nucleus and activating Nrf2/ARE signalling in the type 2 diabetic KK-Ay mice model. This evidence concerns the gene SLC5A2 and Myocardial fibrosis.