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Fig. 9 | Particle and Fibre Toxicology

Fig. 9

From: Zinc oxide nanoparticles effectively regulate autophagic cell death by activating autophagosome formation and interfering with their maturation

Fig. 9

Schematic of the proposed mechanisms of ZnO NPs-inducing autophagic cell death in PC12 cells. ZnO NPs are delivered into lysosomes, and subsequently dissolved in lysosomes to release zinc ions. Zinc ions (intracellular or extracellular) is the crucial factor triggering oxidative stress. Furthermore, the JNK is activated in response to cellular ROS, and JNK activation promotes the initiation of autophagy by phosphorylating Bcl-2, leading to the release of Beclin 1 from Bcl-2. Autophagy is a process of lysosomal-mediated cellular self-digestion. In addition, when the expression of autophagosomal-lysosomal fusion related protein LAMP-2 was affected by excessive zinc ions, autophagic flux will be significantly impaired, aggravating the accumulation of autophagosomes and then inducing autophagic stress. Furthermore, autophagy is also involved in transporting ZnO NPs into lysosomes, accelerating ROS production, enhancing JNK activation, and finally increasing autophagy to form a positive feedback mechanism that contributes to ZnO NPs-induced autophagic cell death

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