Functional interaction of endoplasmic reticulum stress and hepatitis B virus in the pathogenesis of liver diseases

Figure 1 Endoplasmic reticulum stress and unfolded protein response signaling pathways. ER: Endoplasmic reticulum; BIP: Binding immunoglobulin protein; PERK: Protein kinase RNA-like ER kinase; eIF2α: Eukaryotic translational initiation factor 2α; ATF4: Activating transcription factor 4; IRE1: Inositol-requiring protein 1; XBP1: X-box binding protein 1; ATF6: Activating transcription factor 6; S1P: Site 1 protease; S2P: Site 2 protease; UPR: Unfolded protein response; ERAD: ER associated degradation; CHOP: C/EBP homologous protein; P: Phosphate.

Figure 2 Mechanisms for the pathogenesis of hepatitis B virus-induced liver diseases via mitochondrial damage and endoplasmic reticulum stress. Plus and minus symbols are up- and down-regulated responses, respectively. HBV: Hepatitis B virus; cccDNA: Covalently closed circular DNA; ER: Endoplasmic reticulum; HBx: Hepatitis B virus X protein; ROS: Reactive oxygen species; ATF4: Activating transcription factor 4; XBP1: X-box binding protein 1; ATF6: Activating transcription factor 6.