Park SC, Kim YJ, Kim JW. Targeting uridine diphosphate glucuronosyltransferase 1A1 in liver disease: Current research and future directions. World J Gastroenterol 2024; 30(39): 4305-4307 [PMID: 39492821 DOI: 10.3748/wjg.v30.i39.4305]
Corresponding Author of This Article
Jong-Won Kim, PhD, Center for Pharmacogenetics and Department of Pharmaceutical Sciences, University of Pittsburgh, 335 Sutherland Dr., Pittsburgh, PA 15216, United States. jok148@pitt.edu
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): 4305-4307 Published online Oct 21, 2024. doi: 10.3748/wjg.v30.i39.4305
Targeting uridine diphosphate glucuronosyltransferase 1A1 in liver disease: Current research and future directions
Seok-Chan Park, Yu Ji Kim, Jong-Won Kim
Seok-Chan Park, Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, United States
Yu Ji Kim, Division of Endocrinology and Metabolism, Department of Internal Medicine, Medical School, Jeonbuk National University, Research Institute of Clinical Medicine of Jeonbuk National University-Biomedical Research Institute of Jeonbuk National University Hospital, Jeonju 54907, South Korea
Jong-Won Kim, Center for Pharmacogenetics and Department of Pharmaceutical Sciences, University of Pittsburgh, Pittsburgh, PA 15216, United States
Co-corresponding authors: Yu Ji Kim and Jong-Won Kim.
Author contributions: Park SC wrote the original draft; Kim YJ and Kim JW contributed to conceptualization, writing, reviewing, and editing; Kim YJ and Kim JW participated in drafting the manuscript; and all authors have read and approved the final version of the manuscript.
Supported byThe Fund of Biomedical Research Institute, Jeonbuk National University Hospital, The Korea Health Technology R and D Project through the Korea Health Industry Development Institute (KHIDI), No. HI22C2101 and No. HI20C0209.
Conflict-of-interest statement: The authors declare no competing financial interests.
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: Jong-Won Kim, PhD, Center for Pharmacogenetics and Department of Pharmaceutical Sciences, University of Pittsburgh, 335 Sutherland Dr., Pittsburgh, PA 15216, United States. jok148@pitt.edu
Received: May 7, 2024 Revised: September 19, 2024 Accepted: September 25, 2024 Published online: October 21, 2024 Processing time: 158 Days and 0.8 Hours
Abstract
The current letter to the editor pertains to the manuscript entitled 'Uridine diphosphate glucuronosyltransferase 1A1 prevents the progression of liver injury'. Increased levels of uridine diphosphate glucuronosyltransferase 1A1 during liver injury could mitigate damage by reducing endoplasmic reticulum stress, oxidative stress, and dysregulated lipid metabolism, impeding hepatocyte apoptosis and necroptosis.
Core Tip: During liver injury, expression of the uridine diphosphate glucuronosyltransferase (UGT) 1A1 enzyme increases. Interfering with this increase in expression can potentially worsen liver damage. The beneficial effects of UGT1A1 in reducing liver injury might stem from its capacity to alleviate hepatocyte apoptosis and necroptosis, which are driven by endoplasmic reticulum stress, oxidative stress, and abnormal lipid metabolism.
