Kram M. Galectin-3 inhibition as a potential therapeutic target in non-alcoholic steatohepatitis liver fibrosis. World J Hepatol 2023; 15(2): 201-207 [PMID: 36926236 DOI: 10.4254/wjh.v15.i2.201]
Corresponding Author of This Article
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
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Minireviews
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 Hepatol. Feb 27, 2023; 15(2): 201-207 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
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
Abstract
Nonalcoholic fatty liver disease continues to be one of the major health challenges facing the world, with estimates of non-alcoholic steatohepatitis (NASH) prevalence in over 25 percent of the world’s population. NASH represents a spectrum of disease that may lead to hepatic fibrosis and eventual cirrhosis, with the risk of cirrhosis decompensation, and hepatocellular carcinoma. New therapies are desperately needed for NASH, especially for later stages of fibrosis and cirrhosis. Galectin-3 inhibition is being explored as a new liver antifibrotic therapy. This concise review will outline the state of the art of this new therapeutic target.
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.
