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

Figure 1

DM-induced higher basal oxidative state plays a master role in the progression of cardiometabolic disorders and negatively affects the MI/R injury. In this state, ROS and RNS accumulate dramatically. They initiate the reaction of ^∙OH in parallel with the /ONOOH generation, which becomes strong cytotoxic oxidant and causes oxidative damage and nitration. These then lead to endothelium dysfunction, formation of advanced glycation end products, and alteration of the mitochondrial quality control, all contributing to the deleterious MI/R injury in diabetic hearts. Free fatty acid (FFA); protein kinase C-θ (PKC-θ); nuclear factor of kappa light polypeptide gene (NF-κB); superoxide (^∙); hydrogen peroxide (H₂O₂); glutathione peroxidase (GPx); catalase (CAT); hydroxyl (^∙OH); tetrahydrobiopterin (BH4); nitric oxide synthase (NOS); inducible NOS (iNOS); nitric oxide (^∙NO); peroxynitrite (); peroxynitrous acid (ONOOH); nitrogen dioxide (NO₂); mitochondrial permeability transition pore (mPTP).