Fig. 1

Potential mechanisms responsible for cardioprotective effect of SGLT-2 Inhibitors. From current evidence from both in vitro or ex vivo experiments, SGLT-2 inhibitors have been demonstrated that they could have direct cardiac effects on inflammation [63], oxidative stress [65], and ionic dyshomeostasis [116]. Although the effects of SGLT-2 inhibitors on the attenuation of apoptosis and mitochondrial dysfunction could be direct cardiac effects [59, 62, 64], they have not been proved by either in vitro or ex vivo experiments. Italics indicate the mechanisms have not been proved by either in vitro or ex vivo experiments. SGLT-2 sodium–glucose co-transporter 2, NLRP3 nucleotide-binding oligomerization domain-like receptor 3, IL interleukin, STAT3 signal transducer and activator of transcription 3, ERS endoplasmic reticulum stress, Bcl-2 B cell chronic lymphocytic leukemia/lymphoma-2, Bax Bcl-2-associated X, PGC1-α peroxisome proliferator-activated receptor gamma coactivator 1-alpha, CPT1 carnitine palmitoyltransferase 1, ROS reactive oxygen species, NHE Na⁺/H⁺ exchange, [Na⁺]_c cytoplasmic Na⁺ concentration, [Ca²⁺]_c cytoplasmic Ca²⁺ concentration, [Ca²⁺]_m mitochondrial Ca²⁺ concentration, SERCA2a sarcoplasmic endoplasmic reticulum Ca²⁺-ATPase, I/R ischemic/reperfusion