Functional interaction of endoplasmic reticulum stress and hepatitis B virus in the pathogenesis of liver diseases.
Hepatitis B virus (HBV) is a non-cytopathic virus that causes acute and chronic inflammatory liver diseases, often leading to the pathogenesis of hepatocellular carcinoma (HCC). Although many studies for the roles of HBV on pathogenesis of the liver diseases, such as non-alcoholic fatty liver disease (NAFLD), hepatic inflammation, cirrhosis, and HCC, have been reported, the mechanisms are not fully understood. Endoplasmic reticulum (ER) and mitochondria have the protective mechanisms to restore their damaged function by intrinsic or extrinsic stresses, but their chronic dysfunctions are associated with the pathogenesis of the various diseases. Furthermore, HBV can affect intra- or extracellular homeostasis through induction of ER and mitochondrial dysfunctions, leading to liver injury. Therefore, the mechanism by which HBV induces ER or mitochondrial stresses may be a therapeutic target for treatment of liver diseases.
['Kim|So Young|SY|', 'Kyaw|Yi Yi|YY|', 'Cheong|Jaehun|J|']
D000818:Animals D000998:Antiviral Agents D002908:Chronic Disease D004195:Disease Models, Animal D004721:Endoplasmic Reticulum D059865:Endoplasmic Reticulum Stress D006515:Hepatitis B virus D006801:Humans D008099:Liver D008107:Liver Diseases D008928:Mitochondria D015398:Signal Transduction D056811:Unfolded Protein Response D053586:Virus Internalization D014779:Virus Replication
Endoplasmic reticulum stress Hepatitis B virus Liver disease Hepatitis B virus X protein Unfolded protein response