Oxidative stress signaling underlying liver disease and hepatoprotective mechanisms

Figure 1 Interrelationships between the level of oxidative stress and insulin resistance, leading to hepatic steatosis and its progression to steatohepatitis, associated with overnutrition. AP-1: Activating protein 1; CYP2E1: Ethanol inducible form of cytochrome P450; FA: Fatty acids; IL-1: Interleukin-1; LCPUFA; Long-chain polyunsaturated fatty acids; NF-κB: Nuclear factor-κB; NOX2: NADPH oxidase in phagocytic cells; PPAR-α: Peroxisome proliferator-activated receptor-α; ROS: Reactive oxygen species; SREBP-1c: Sterol regulatory element binding protein-1c; TNF-α: Tumor necrosis factor-α.

Figure 2 Oxidative stress signaling in thyroid hormone (T3) liver preconditioning as mediated by redox-sensitive transcriptional factors NF-κB, AP-1, and STAT3 (A) or Nrf2 (B). AP-1: Activating protein 1; ARE: Antioxidant responsive element; GdCl3: Gadolinium chloride; IL: Interleukin; iNOS: Inducible nitric oxide synthase; MnSOD: Manganese superoxide dismutase; NF-κB: Nuclear factor-κB; Nrf2: Nuclear factor-erythroid 2-related factor 2; QO2: Rate of oxygen consumption; TNF-α: Tumor necrosis factor-α; STAT3: Signal transducer and activator of transcription 3; TR: Thyroid hormone receptor; UCP: Uncoupling protein.