Molecular mechanism of nanomaterials induced liver injury: A review

Figure 2 Diagram showing nanoparticles induced hepatotoxicity through inflammatory pathway and its crosstalk with oxidative stress, endoplasmic reticulum stress and apoptotic pathways. AP1: Activator protein 1; Apaf-1: Apoptotic peptidase activating factor 1; ASK1: Apoptosis signal-regulating kinase 1; ATF3/4: Activating transcription factor 3/4; BAK: Bcl-2 homologues antagonist/killer; Bax: Bcl-2-associated X-protein; Bcl2: B-cell lymphoma 2; BclXL: B-cell lymphoma-extra-large; Bim: Bcl-2 interacting mediator of cell death; Ca++: Calcium ion; Casp 1/3/6/7/9/12: Caspase 1/3/6/7/9/12; CHOP: C/EBP Homologous Protein; CytC: Cytochrome C; eIF2α: Eukaryotic initiation factor 2 alpha; GSDMS: Gasdermins; IKK: IκB kinase; Iκβ: Inhibitor of nuclear factor kappa beta; IL-6/18: Interleukin 6/18; IL-1β: Interleukin 1 β; IRE1: Inositol-requiring enzyme type 1; JNK: Jun N-terminal kinase; mtROS: Mitochondrial reactive oxygen species; NFkβ: Nuclear factor kappa beta; NLRP3: NOD-like receptor protein 3; NOXA: Phorbol-12-myristate-13-acetate-induced protein 1; NPs- Nanoparticles; p53: Tumor suppressor protein p53; PERK: Protein kinase RNA like endoplasmic reticulum kinase; Pro-Casp 1: Pro- Caspase 1; Pro-IL-18: Pro- Interleukin 18; Pro-IL-1β: Pro- Interleukin 1 β; PUMA- p53 upregulated modulator of apoptosis; ROS: Reactive Oxygen Species; TNFR: Tumor necrosis factor receptor; TNFα: Tumor necrosis factor alpha; TRAF2: TNF receptor associated factor 2.