Xu-Dong Feng, MD, PhD, Doctor, Department of Clinical Laboratory, Ningbo Medical Center Lihuili Hospital, The Affiliated Lihuili Hospital of Ningbo University, No. 57 Xingning Road, Ningbo 315000, Zhejiang Province, China. xdfeng@zju.edu.cn
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Letter to the Editor
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. Oct 21, 2024; 30(39): 4308-4312 Published online Oct 21, 2024. doi: 10.3748/wjg.v30.i39.4308
Novel intervention for alcohol-associated liver disease
Fei-Qiong Gao, Jia-Qi Zhu, Xu-Dong Feng
Fei-Qiong Gao, Department of Endocrinology, The Affiliated Hangzhou First People's Hospital, School of Medicine, Westlake University, Hangzhou 310003, Zhejiang Province, China
Jia-Qi Zhu, Laboratory Medicine Center, Department of Clinical Laboratory, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou 310014, Zhejiang Province, China
Xu-Dong Feng, Department of Clinical Laboratory, Ningbo Medical Center Lihuili Hospital, The Affiliated Lihuili Hospital of Ningbo University, Ningbo 315000, Zhejiang Province, China
Author contributions: Gao FQ and Feng XD conceived the idea of the manuscript; Gao FQ wrote the draft; Zhu JQ reviewed the literature; Feng XD revised the manuscript; all authors approved the final manuscript.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
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: Xu-Dong Feng, MD, PhD, Doctor, Department of Clinical Laboratory, Ningbo Medical Center Lihuili Hospital, The Affiliated Lihuili Hospital of Ningbo University, No. 57 Xingning Road, Ningbo 315000, Zhejiang Province, China. xdfeng@zju.edu.cn
Received: July 20, 2024 Revised: August 27, 2024 Accepted: September 19, 2024 Published online: October 21, 2024 Processing time: 84 Days and 0.6 Hours
Abstract
A recently published article in the World Journal of Gastroenterology clarified that elafibranor, a dual peroxisome proliferator activated receptor α/δ (PPARα/δ) agonist, reduced inflammation and fibrosis in alcohol-associated liver disease (ALD). This letter aims to discuss the findings presented in that article. ALD is a global health problem, and no effective drugs has been approved by the Food and Drug Administration to cure it. Thus, finding targeted therapies is of great urgency. Herein, we focus on the pathogenesis of ALD and the role of PPARα/δ in its development. Consistent with the conclusion of the article of interest, we think that elafibranor may be a promising therapeutic option for ALD, due to the pivotal involvement of PPARα/δ in the pathogenesis of the disease. However, its treatment dose, timing, and side effects need to be further investigated in future studies.
Core Tip: Alcohol-associated liver disease (ALD) remains a significant global health challenge. Peroxisome proliferator-activated receptors α and δ (PPARα/δ) play a crucial role in the pathogenesis of ALD. Elafibranor, a dual PPARα/δ activator, shows promise as a potential therapeutic agent for ALD.
