FA deficiency simultaneously enhanced the activity of autophagy and induced the generation of oxidative stress following the MCAO model; oxidative injury seems to be involved in excessive activation of autophagy caused by FA deficiency.
Autophagy is upregulated, and the level of ROS is elevated in the central nervous system after ischemia-reperfusion; Antioxidants can protect neural cells and decrease infarct volume possibly by activating the autophagic pathway of cells.
Chemical inhibitors of autophagy or lysosomes can delay the release of mitochondrial ROS to prolong the therapeutic time window. Ischemic insults will immediately initiate autophagy induction with undefined mechanisms, which significantly will impact ROS production and oxidative damage in vivo.
Sirt3 showed a protective role in eliminating intracellular H2O2, attenuating mitochondrial O2−, and promoting autophagy through the AMPK-mTOR pathway in neuronal ischemia.
SIRT6-mediated autophagy contributes to oxidative stress-induced neuronal injury since inhibition of autophagy could prevent the detrimental effect of SIRT6 on cell survival, which could be attributed to attenuation of AKT signaling closely related to oxidative stress.
The autophagic removal of Aβ mediated by Parkin can attenuate oxidative stress and mitochondrial dysfunction to restore energy supply for a better modulation of autophagy in AD transgenic mice.
Autophagy is proposed as an antioxidant protective pathway that can clear cumulative ROS and reverse established ROS-induced protein, DNA, and lipid damage independent of the disposal of radical scavengers.
Autophagy can scavenge aggregate-prone proteins and increased ROS, while antioxidants can block autophagy and thereby counterbalance the benefits of autophagy and exacerbate neurodegeneration.
Loss of PINK1 function can stir oxidative stress, which can then elicit coordinated autophagy and mitophagy for mitochondrial turnover by a removal of dysfunctional mitochondria.
