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In doxorubicin-induced cardiotoxicity, FNDC5/irisin alleviates oxidative stress and cardiomyocyte apoptosis by activating AKT/mTOR signaling and the AKT/GSK3/FYN/Nrf2 axis [197]

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Chronic hyperglycemia results in the suppressed activity of mTOR associated with AMP-activated protein kinase-induced increase in ROS formation and enhanced expression of thioredoxin interacting protein (TXNIP) a potential sensor of glucose and oxidative stress (Akpoveso et al