Shahram Golbabapour, Kamran Bagheri-Lankarani, Saeid Ghavami and Bita Geramizadeh* Pages 6073 - 6095 ( 23 )
Autoimmune hepatitis is a necroinflammatory process of liver, featuring interface hepatitis by T cells, macrophages and plasma cells that invade to periportal parenchyma. In this process, a variety of cytokines are secreted and liver tissues undergo fibrogenesis, resulting in the apoptosis of hepatocytes. Autophagy is a complementary mechanism for restraining intracellular pathogens to which the innate immune system does not provide efficient endocytosis. Hepatocytes with their particular regenerative features are normally in a quiescent state, and, autophagy controls the accumulation of excess products, therefore the liver serves as a basic model for the study of autophagy. Impairment of autophagy in the liver causes the accumulation of damaged organelles, misfolded proteins and exceeded lipids in hepatocytes as seen in metabolic diseases. In this review, we introduce autoimmune hepatitis in association with autophagy signaling. We also discuss some genes and proteins of autophagy, their regulatory roles in the activation of hepatic stellate cells and the importance of lipophagy and tyrosine kinase in hepatic fibrogenesis. In order to provide a comprehensive overview of the regulatory role of autophagy in autoimmune hepatitis, the pathway analysis of autophagy in autoimmune hepatitis is also included in this article.
Autoimmune hepatitis, stellate cells, autophagy, cell signaling, autoimmune diseases, AIH, chronic hepatitis.
Rheumatology Research Group, Institute of Inflammation and Ageing, University of Birmingham, Queen Elizabeth Hospital, Birmingham, B15 2WB, Health Policy Research Center, Institute of Health, Shiraz University of Medical Sciences, Shiraz, Health Policy Research Center, Institute of Health, Shiraz University of Medical Sciences, Shiraz, Department of Pathology, Medical school of Shiraz University, Shiraz University of Medical Sciences, Shiraz