Basic Study
Copyright ©The Author(s) 2023. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jun 14, 2023; 29(22): 3422-3439
Published online Jun 14, 2023. doi: 10.3748/wjg.v29.i22.3422
Mechanism of annexin A1/N-formylpeptide receptor regulation of macrophage function to inhibit hepatic stellate cell activation through Wnt/β-catenin pathway
Jun-Hua Fan, Na Luo, Geng-Feng Liu, Xiao-Fang Xu, Shi-Quan Li, Xiao-Ping Lv
Jun-Hua Fan, Na Luo, Geng-Feng Liu, Xiao-Fang Xu, Shi-Quan Li, Xiao-Ping Lv, Department of Gastroenterology, The First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi Zhuang Autonomous Region, China
Author contributions: Fan JH, Luo N and Liu GF performed most of the experiments; Luo N, Xu XF and Li SQ analyzed the data; Fan JH and Lv XP designed the study and wrote the paper.
Supported by a Grant-in-Aid for Scientific Research from National Natural Science Foundation of China, No. 81860120 and 81860104; Guangxi Natural Science Foundation, No. 2017GXNSFBA198134, 2017GXNSFAA198299 and 2015GXNSFCA139024.
Institutional animal care and use committee statement: All experiments were conducted in accordance with the institutional guidelines of Guangxi Medical University for the care and use of laboratory animals.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Data sharing statement: No additional data are available.
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: Jun-Hua Fan, Doctor, MD, PhD, Associate Professor, Doctor, Department of Gastroenterology, The First Affiliated Hospital of Guangxi Medical University, No. 6 Shuangyong Road, Nanning 530021, Guangxi Zhuang Autonomous Region, China. fanjunhuaxiaoshe@hotmail.com
Received: February 15, 2023
Peer-review started: February 15, 2023
First decision: March 28, 2023
Revised: April 10, 2023
Accepted: May 11, 2023
Article in press: May 11, 2023
Published online: June 14, 2023
ARTICLE HIGHLIGHTS
Research background

Liver fibrosis is a pathological change caused by chronic liver injury, and is a key link in the progression of chronic liver diseases to cirrhosis or liver cancer. How to prevent and reverse liver fibrosis is currently a hot and difficult research topic, and fully understanding and elucidating the pathogenesis of liver fibrosis is the foundation of prevention and treatment. At present, there is still a lack of safe and effective treatment for liver cirrhosis clinically. It is of great significance to deeply study the pathogenesis of liver fiber and prevent and treat it in order to reduce the incidence rate and mortality of liver cirrhosis.

Research motivation

Studies have shown that liver fibrosis is closely related to inflammation in chronic liver disease, and annexin (Anx)A1 has strong anti-inflammatory effects. Therefore, this study focuses on the pathogenesis of liver fibrosis and investigates the role of AnxA1 in liver fibrosis. Provide valuable information for antifibrosis therapy.

Research objectives

To investigate molecular and cellular mechanisms of liver fibrosis and evaluate the effect of AnxA1 in hepatic fibrosis.

Research methods

Biomarkers as drug development tools, biomarker discovery and validation using a combination of in vitro and in vivo studies. A large and wide range of animal models and cell experiments can be used, and experiments can be repeated multiple times.

Research results

AnxA1/formylpeptide receptor (FPR) inhibits the activation of hepatic stellate cells by regulating macrophage function through the Wnt/β-catenin pathway in the CCl4-induced hepatic fibrosis mice.

Research conclusions

AnxA1 may involve in the pathogenesis of liver fibrosis and as a potential therapeutic target.

Research perspectives

This study investigates the mechanism of Anxa1 in liver fibrosis by using wild mice/Anxa1 knockout mice in combination with Anxa1 mimetic peptide and FPR receptor inhibitor to provide an experimental basis for the possible use of Anxa1 in the treatment of liver fibrosis.