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World J Gastroenterol. Nov 21, 2017; 23(43): 7657-7665
Published online Nov 21, 2017. doi: 10.3748/wjg.v23.i43.7657
Functional interaction of endoplasmic reticulum stress and hepatitis B virus in the pathogenesis of liver diseases
So Young Kim, Yi Yi Kyaw, Jaehun Cheong
So Young Kim, Yi Yi Kyaw, Jaehun Cheong, Department of Molecular Biology, Pusan National University, Busan 609-735, South Korea
Author contributions: Kim SY and Kyaw YY prepared the manuscript; Cheong J designed and revised the manuscript.
Supported by the National Research Foundation of South Korea, No. NRF-2009-0093195; and Basic Science Research Program through the NRF funded by the Ministry of Education, No. NRF-2013R1A1A2057634.
Conflict-of-interest statement: The authors declare that they have no conflict of interest.
Correspondence to: Jaehun Cheong, PhD, Department of Molecular Biology, Pusan National University, Busan 609-735, South Korea. molecule85@pusan.ac.kr
Telephone: +82-51-5102277 Fax: +82-51-5139258
Received: April 21, 2017
Peer-review started: April 25, 2017
First decision: June 22, 2017
Revised: September 1, 2017
Accepted: November 1, 2017
Article in press: November 1, 2017
Published online: November 21, 2017
Processing time: 212 Days and 11.1 Hours
Core Tip

Core tip: Endoplasmic reticulum (ER) is the major site of protein folding and calcium storage. Beside the role of ER in protein homeostasis, it controls the cholesterol production and lipid-membrane biosynthesis as well as surviving and cell death signaling mechanisms in the cell. It is well-documented that abnormal metabolic regulation induces adverse effects in liver disorders, such as non-alcoholic steatosis hepatitis, fibrosis, cirrhosis, and hepatocellular carcinoma which are associated with hepatitis B virus (HBV) infection. Recent animal model and human studies have showed ER stress as an emerging factors involved in the development of metabolic and liver diseases. In this review, we will summarize the crucial effects of ER stress response in the pathogenesis of HBV-induced liver diseases.