Title:Autoimmune Hepatitis and Stellate Cells: An Insight into the Role of Autophagy
Volume: 27
Issue: 35
Author(s): Shahram Golbabapour, Kamran Bagheri-Lankarani, Saeid Ghavami and Bita Geramizadeh*
Affiliation:
- Department of Pathology, Medical school of Shiraz University, Shiraz University of Medical Sciences, Shiraz,Iran
Keywords:
Autoimmune hepatitis, stellate cells, autophagy, cell signaling, autoimmune diseases, AIH, chronic
hepatitis.
Abstract: 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.
