Zhang JW. Role of 1,25-dihydroxyvitamin D3 in alleviating hepatic steatosis: Targeting M1 macrophage polarization in non-alcoholic fatty liver disease. World J Gastrointest Oncol 2025; 17(3): 102424 [DOI: 10.4251/wjgo.v17.i3.102424]
Corresponding Author of This Article
Jin-Wei Zhang, BSc, MSc, PhD, Academic Editor, Professor, Senior Editor, State Key Laboratory of Chemical Biology, Research Center of Chemical Kinomics, Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, No. 345 Lingling Road, Shanghai 200032, China. jinweizhang@sioc.ac.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 Gastrointest Oncol. Mar 15, 2025; 17(3): 102424 Published online Mar 15, 2025. doi: 10.4251/wjgo.v17.i3.102424
Role of 1,25-dihydroxyvitamin D3 in alleviating hepatic steatosis: Targeting M1 macrophage polarization in non-alcoholic fatty liver disease
Jin-Wei Zhang
Jin-Wei Zhang, State Key Laboratory of Chemical Biology, Research Center of Chemical Kinomics, Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, Shanghai 200032, China
Author contributions: Zhang JW designed the overall concept and outline of the manuscript; Zhang JW contributed to the discussion and design of the manuscript; Zhang JW contributed to the writing and editing of the manuscript, illustrations, and review of the literature.
Supported by National Natural Science Foundation of China, No. 82170406 and No. 81970238.
Conflict-of-interest statement: Dr. Zhang declares that he has no conflict of interest to disclose.
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: Jin-Wei Zhang, BSc, MSc, PhD, Academic Editor, Professor, Senior Editor, State Key Laboratory of Chemical Biology, Research Center of Chemical Kinomics, Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, No. 345 Lingling Road, Shanghai 200032, China. jinweizhang@sioc.ac.cn
Received: October 17, 2024 Revised: November 30, 2024 Accepted: December 17, 2024 Published online: March 15, 2025 Processing time: 120 Days and 7.3 Hours
Abstract
Non-alcoholic fatty liver disease (NAFLD), a critical global health concern, continues to challenge medical researchers with limited treatment options. This letter examines on the study by Luo et al, demonstrating that vitamin D 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] improves hepatic steatosis in NAFLD by inhibiting M1 macrophage polarization via the vitamin D receptor-peroxisome proliferator-activated receptor gamma signaling pathway. This letter critically appraises these findings, comparing them to similar studies, and discusses their potential implications for treating NAFLD. Furthermore, we highlight future directions, including dose optimization and mechanistic studies.
Core Tip: This letter critically analyzes the study by Luo et al, on the effects of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] in reducing lipid accumulation in hepatocytes by inhibiting M1 macrophage polarization through the vitamin D receptor-peroxisome proliferator-activated receptor gamma pathway in non-alcoholic fatty liver disease (NAFLD). The study highlights how 1,25(OH)₂D₃ improves lipid metabolism and reduces inflammation, offering promising insights for NAFLD treatment. Future research should focus on dose optimization, detailed molecular mechanisms, and translating findings into human clinical trials to validate vitamin D's therapeutic potential in managing NAFLD.
