Figure 8.

Schematic model of the underlying mechanism of autophagy dysfunction induced by SiNPs.

Notes: SiNPs can be endocytosed into L-02 and HepG2 cells and trigger autophagy through ROS. Moreover, SiNPs were largely deposited in lysosomes and impaired lysosomal function through destroying lysosomal ultrastructures, increasing membrane permeability, and downregulating the expression of lysosomal proteases. Eventually, SiNPs blocked the autophagic flux and caused autophagy dysfunction.

Abbreviations: CTSB, cathepsin B; ROS, reactive oxygen species; SiNPs, silica nanoparticles.