Kim SY, Kyaw YY, Cheong J. Functional interaction of endoplasmic reticulum stress and hepatitis B virus in the pathogenesis of liver diseases. World J Gastroenterol 2017; 23(43): 7657-7665 [PMID: 29209107 DOI: 10.3748/wjg.v23.i43.7657]
Corresponding Author of This Article
Jaehun Cheong, PhD, Department of Molecular Biology, Pusan National University, Busan 609-735, South Korea. molecule85@pusan.ac.kr
Research Domain of This Article
Virology
Article-Type of This Article
Minireviews
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
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.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
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.
