Basic Study
Copyright ©The Author(s) 2022. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jul 14, 2022; 28(26): 3201-3217
Published online Jul 14, 2022. doi: 10.3748/wjg.v28.i26.3201
Intracellular alpha-fetoprotein mitigates hepatocyte apoptosis and necroptosis by inhibiting endoplasmic reticulum stress
Yun-Fen Chen, Si-Ying Liu, Qi-Jiao Cheng, Yu-Jiao Wang, Shuang Chen, Yi-Yang Zhou, Xia Liu, Zhi-Gang Jiang, Wei-Wei Zhong, Yi-Huai He
Yun-Fen Chen, Si-Ying Liu, Qi-Jiao Cheng, Shuang Chen, Yi-Yang Zhou, Xia Liu, Yi-Huai He, Department of Infectious Diseases, The Affiliated Hospital of Zunyi Medical University, Zunyi 563000, Guizhou Province, China
Yu-Jiao Wang, Department of General Medicine, The Affiliated Hospital of Zunyi Medical University, Zunyi 563000, Guizhou Province, China
Zhi-Gang Jiang, School of Public Health, Zunyi Medical University, Zunyi 563099, Guizhou Province, China
Wei-Wei Zhong, Department of Endoscopy, Jingmen No.1 People’s Hospital, Jingmen 448000, Hubei Province, China
Author contributions: Chen YF, Liu SY, and Cheng QJ contributed equally to this work; Chen YF, Liu SY, Cheng QJ, and He YH conceived and designed research; Chen YF, Liu SY, Wang YJ, Chen S, Zhou YY, and Liu X collected data and conducted research; Jiang ZG, Chen YF, and Zhong WW analyzed and interpreted data; Chen YF, Liu SY, and Cheng QJ wrote the initial paper; He YH and Zhong WW revised the paper; He YH had primary responsibility for final content; all authors read and approved the final manuscript.
Supported by the National Natural Science Foundation of China, No. 81560110; Tian Qing Liver Disease Research Fund Project of the Chinese Foundation for Hepatitis Prevention and Control, No. TQGB20200001; and the Science and Technology Planning Projects of Guizhou Province and Zunyi City, No. QKH·ZC[2019] 2803, No. QKHJC-ZK[2022]YB642, No. QKH·PTRC[2017]5733-013, No. gzwjkj2020-1-041, No. ZSKHSZ[2020]230, and No. ZMC·YZ[2018]38.
Institutional review board statement: The study was reviewed and approved by the Ethics Committee of Affiliated Hospital of Zunyi Medical University (ZYFYLS[2018] 28).
Institutional animal care and use committee statement: All procedures involving animals were reviewed and approved by the Animal Experiment Ethics Committee of Zunyi Medical University (LS[2020] 2-231).
Conflict-of-interest statement: There are no conflicts of interest to report.
Data sharing statement: The datasets generated and analyzed during the current study are available from the corresponding author on reasonable request.
ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (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: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Yi-Huai He, MM, Director, Department of Infectious Diseases, The Affiliated Hospital of Zunyi Medical University, No. 201 Dalian Street, Zunyi 563000, Guizhou Province, China. 993565989@qq.com
Received: January 13, 2022
Peer-review started: January 13, 2022
First decision: March 8, 2022
Revised: March 22, 2022
Accepted: May 13, 2022
Article in press: May 13, 2022
Published online: July 14, 2022
Core Tip

Core Tip: During the process of liver injury, alpha-fetoprotein (AFP) expression was up-regulated in hepatocytes, especially in the necrotic areas, but it did not increase the serum AFP level. Endoplasmic reticulum (ER) stress induced intracellular AFP expression through activating activating transcription factor-6 and the up-regulated intracellular AFP expression attenuated hepatocyte apoptosis and necroptosis by feedback-down-regulating ER stress.