Figure 7.

A schematic model for SIRT3-induced autophagy and its underlying mechanism in SH-SY5Y cells following rotenone treatment. SIRT3 overexpression leads to an acceleration of LKB1 activation (phosphorylation) and downstream AMPK activation, thus decreasing mTOR phosphorylation and initiating an autophagic response. In a rotenone-induced Parkinson cell model, there is enhanced α-synuclein aggregation, accelerated oxidative stress and increased mitochondria dysfunction. With SIRT3 overexpression and induced autophagic levels, these injuries are ameliorated. Blocking autophagy using 3-MA abolished the protective effect. Our results suggest that SIRT3 protects cells from rotenone by generating autophagy. The LKB1-AMPK-mTOR pathway is involved in the generation.