In a mouse post-MI HFrEF model: empagliflozin treatment improved cardiac remodeling by the inhibition of apoptosis, alleviated oxidative stress, restored mitochondrial membrane potential, and activated AMPK signaling [83]; dapagliflozin treatment inhibited cardiac apoptosis and reduced LV mass, the expression of cardiac collagen 1/3, atrial natriuretic peptide (ANP), B-type natriuretic peptide (BNP), and transforming growth factor-β1 (TGF-β1) transcripts of cardiac fibrosis histological staining [77]. The gene discussed is TGFB1; the disease is myocardial infarction.