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Fig. 3 | Journal of Nanobiotechnology

Fig. 3

From: Nanomaterials and hepatic disease: toxicokinetics, disease types, intrinsic mechanisms, liver susceptibility, and influencing factors

Fig. 3

Schematic of the main mechanisms of NM-induced NASH. NM exposure induced persistent stimuli, such as cytokines, lipid peroxides and molecules, from activated KCs, and injured hepatocytes induce HSC activation, leading to fibrogenesis or even cirrhosis. Exposure to NMs (SiO2-, TiO2-, and ZnO-NPs) induces NASH via hepatic IR, which is triggered by ROS-mediated inflammation activated by the MAPK and NF-κB pathways. The activation of KCs by NMs (carbon black NPs, graphene NPs, SIPONs, Cu- NPs, SiO2- NPs, and TiO2-NPs) also contributes to IR and lipotoxicity in hepatocytes via the release of cytokines and chemokines

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