Insights for Oxidative Stress and mTOR Signaling in Myocardial Ischemia/Reperfusion Injury under Diabetes

Figure 2

The diabetic heart is susceptible to MI/R injury. Impaired activation of prosurvival pathways, endoplasmic reticulum (ER) stress, increased basal oxidative state, and decreased antioxidant defense and autophagy may render diabetic hearts to be more vulnerable to MI/R injury and be resistant to ischemic preconditioning (IPC) or ischemic postconditioning (I-post). Oxidative stress and mTOR signaling crucially regulate cardiometabolism, affecting MI/R injury under diabetes. Reperfusion injury salvage kinase (RISK); phosphoinositide-3 kinase (PI3k); glycogen synthase kinase-3β (GSK-3β); signal transducer and activator of transcription (STAT); autophagy related gene 13 (Atg13); mammalian Atg1 homologues UNC-51-like kinase (ULK); Janus kinase 2 (JAK2); extracellular regulated MAP kinase (ERK).