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22 ChengJ

doi: 10.1369/jhc.2009.953190

In addition to increasing oxidative stress, dysfunctional -ketoglutarate dehydrogenase increases mitochondrial free radical-induced damage and ETC inhibition, further increasing ROS production and initiating apoptotic pathways [61]

Our findings are consistent with a recent study indicating rapamycin-sensitive expression of xCT in TSC models, which the authors attribute to the OCT1 transcription factor (Li et al., 2019)

[168], he proposed that NO may bind to the enzymes of mitochondrial ETC, such as NADH succinate oxidoreductase, NADH ubiquinone oxidoreductase, and cis aconitase and induce uncoupling of OXPHOS followed by the inhibition of glycolysis [66] and depletion of ATP in the cells [169]