Table of Contents
Hepatitis Research and Treatment
Volume 2010, Article ID 205128, 10 pages
Review Article

Biliary Epithelial Apoptosis, Autophagy, and Senescence in Primary Biliary Cirrhosis

Department of Human Pathology, Kanazawa University Graduate School of Medicine, Kanazawa 920-8640, Japan

Received 28 August 2010; Accepted 5 October 2010

Academic Editor: Annarosa Floreani

Copyright © 2010 Motoko Sasaki and Yasuni Nakanuma. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Primary biliary cirrhosis (PBC) is a chronic cholestatic liver disease characterized serologically by the high prevalence of anti-mitochondrial autoantibodies (AMAs) and histologically by the cholangitis of small bile ducts, eventually followed by extensive loss of the small bile duct. An autoimmune pathogenesis is suggested by clinical and experimental studies, but there remain issues regarding the etiology, the significance of AMAs in the pathogenesis of bile duct lesions, and so on. The unique properties of apoptosis in biliary epithelial cells (BECs), in which there is exposure of autoantigen to the effectors of the immune system, are proposed to be a cause of bile duct lesions in PBC. Recent progress disclosed that cellular senescence and autophagy are involved in bile duct lesions in PBC. Senescent BECs may modulate the periductal microenvironment by expressing senescence-associated secretory phenotypes, including various chemokines, and contribute to the pathogenesis of bile duct lesions in PBC.