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Fig. 4 | Journal of Nanobiotechnology

Fig. 4

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

Fig. 4

Schematic of the progression and main mechanisms of NM-induced hepatic fibrosis. Cu-, TiO2- and NiO-NPs induce HSC activation by stimulating TGF-β/SMAD-dependent and TGF-β/SMAD-independent (i.e., MAPK/WNT and AKT/FOXO3) signaling, leading to liver fibrosis. Si- and Cu-NPs induce HSC activation by activating TLR4/MYD88/NF-κB signaling. Graphene QDs and Ni-NPs induce HSC activation by upregulating miR‑21 expression then activating MMP2, 9 expression. Activation of TGF-β (induced by Cu-, TiO2- and NiO-NP), STAT3 (triggered by Cu- and Si-NPs), and IL-4 and IL-13 (induced by SPIONs and MWNTs) induces HSC activation by triggering M1-M2 polarization of KCs

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