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. 2020 Aug 14;11(8):630. doi: 10.1038/s41419-020-02866-3

Fig. 8. Schematic diagram for the role of autophagy in silibinin-induced mitochondrial damage and AIF-dependent glioma cell death.

Fig. 8

Silibinin inhibits glycolysis in glioma cells, which results in autophagy activation. The activated autophagy selectively degrades Δ133p53α (an inhibitoryp 53 isoform) to improve p53 phosphorylation. Then, the phosphorylated p53 reinforces generation of hydrogen peroxide, which further promotes the expression of BNIP3. BNIP3 damages mitochondria and causes AIF translocate from mitochondrion into nucleus. Finally, AIF leads to cell death via causing chromatinolysis.