Fujii J, Homma T, Kobayashi S, Seo HG. Mutual interaction between oxidative stress and endoplasmic reticulum stress in the pathogenesis of diseases specifically focusing on non-alcoholic fatty liver disease. World J Biol Chem 2018; 9(1): 1-15 [PMID: 30364769 DOI: 10.4331/wjbc.v9.i1.1]
Corresponding Author of This Article
Junichi Fujii, PhD, Professor, Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Yamagata University, 2-2-2 Iidanishi, Yamagata City, Yamagata 990-9585, Japan. jfujii@med.id.yamagata-u.ac.jp
Research Domain of This Article
Biochemistry & Molecular Biology
Article-Type of This Article
Review
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 Biol Chem. Oct 18, 2018; 9(1): 1-15 Published online Oct 18, 2018. doi: 10.4331/wjbc.v9.i1.1
Mutual interaction between oxidative stress and endoplasmic reticulum stress in the pathogenesis of diseases specifically focusing on non-alcoholic fatty liver disease
Junichi Fujii, Takujiro Homma, Sho Kobayashi, Han Geuk Seo
Junichi Fujii, Takujiro Homma, Sho Kobayashi, Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Yamagata University, Yamagata 990-9585, Japan
Han Geuk Seo, Sanghuh College of Life Sciences, Konkuk University, Seoul 143-701, South Korea
Author contributions: Fujii J and Seo HG have mainly performed literature review; Homma T and Kobayashi S have largely contributed to experimental data in quoted original papers; based on discussion among them, the idea and the data have been integrated into this review article.
Supported bya Joint Research Project between Japan Society for Promotion of Science and National Research Foundation of South Korea (in part).
Conflict-of-interest statement: We declare no conflict of interest between the authors or with any institution in relation to the contents of this article.
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: Junichi Fujii, PhD, Professor, Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Yamagata University, 2-2-2 Iidanishi, Yamagata City, Yamagata 990-9585, Japan. jfujii@med.id.yamagata-u.ac.jp
Telephone: +81-23-6285227 Fax: +81-23-6285230
Received: July 27, 2018 Peer-review started: July 30, 2018 First decision: August 24, 2018 Revised: September 19, 2018 Accepted: October 11, 2018 Article in press: October 12, 2018 Published online: October 18, 2018 Processing time: 82 Days and 2.6 Hours
Abstract
Reactive oxygen species (ROS) are produced during normal physiologic processes with the consumption of oxygen. While ROS play signaling roles, when they are produced in excess beyond normal antioxidative capacity this can cause pathogenic damage to cells. The majority of such oxidation occurs in polyunsaturated fatty acids and sulfhydryl group in proteins, resulting in lipid peroxidation and protein misfolding, respectively. The accumulation of misfolded proteins in the endoplasmic reticulum (ER) is enhanced under conditions of oxidative stress and results in ER stress, which, together, leads to the malfunction of cellular homeostasis. Multiple types of defensive machinery are activated in unfolded protein response under ER stress to resolve this unfavorable situation. ER stress triggers the malfunction of protein secretion and is associated with a variety of pathogenic conditions including defective insulin secretion from pancreatic β-cells and accelerated lipid droplet formation in hepatocytes. Herein we use nonalcoholic fatty liver disease (NAFLD) as an illustration of such pathological liver conditions that result from ER stress in association with oxidative stress. Protecting the ER by eliminating excessive ROS via the administration of antioxidants or by enhancing lipid-metabolizing capacity via the activation of peroxisome proliferator-activated receptors represent promising therapeutics for NAFLD.
Core tip: Accumulated experimental data indicate that oxidative stress causes endoplasmic reticulum stress, which together leads to pathogenic damage to cells. The lipid metabolism in the liver is a sensitive target of these types of stress, which appears to be associated with non-alcoholic fatty liver disease.
