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©The Author(s) 2023. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Hepatol. Feb 27, 2023; 15(2): 201-207
Published online Feb 27, 2023. doi: 10.4254/wjh.v15.i2.201
Published online Feb 27, 2023. doi: 10.4254/wjh.v15.i2.201
Galectin-3 inhibition as a potential therapeutic target in non-alcoholic steatohepatitis liver fibrosis
Michael Kram, Department of Gastroenterology, Bon Secours Health System Inc, Monsey, NY 10952, United States
Author contributions: Kram M contributed the entire manuscript.
Conflict-of-interest statement: The author reports 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: Michael Kram, MD FACG, Staff Physician, Department of Gastroenterology, Bon Secours Health System Inc, 6 Suhl Lane, Monsey, NY 10952, United States. michaelkrammd@gmail.com
Received: October 6, 2022
Peer-review started: October 6, 2022
First decision: December 12, 2022
Revised: December 17, 2022
Accepted: February 8, 2023
Article in press: February 8, 2023
Published online: February 27, 2023
Processing time: 141 Days and 3.7 Hours
Peer-review started: October 6, 2022
First decision: December 12, 2022
Revised: December 17, 2022
Accepted: February 8, 2023
Article in press: February 8, 2023
Published online: February 27, 2023
Processing time: 141 Days and 3.7 Hours
Core Tip
Core Tip: Galectin-3 inhibition is being advanced as a therapy for liver fibrosis and cirrhosis. Clinicians need to understand the rationale behind this new advance. This minireview will highlight the basic science, as well as recent advances in the field, including the concept of the “galectin-3 fibrosome” and the galectin-3 positive macrophage that enters the liver from the peripheral circulation in the setting of nonalcoholic fatty liver disease. Galectin-3 appears to be central to the non-alcoholic steatohepatitis fibrosis process, and inhibition of galectin-3 is imperative to curtail liver fibrosis.