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World J Gastroenterol. Jul 7, 2020; 26(25): 3577-3585
Published online Jul 7, 2020. doi: 10.3748/wjg.v26.i25.3577
Monoacylglycerol lipase reprograms lipid precursors signaling in liver disease
Matteo Tardelli
Matteo Tardelli, Division of Gastroenterology and Hepatology, Joan and Sanford I Weill Cornell Department of Medicine, Weill Cornell Medical College, New York, NY 10021, United States
Matteo Tardelli, Hans Popper Laboratory of Molecular Hepatology, Division of Gastroenterology and Hepatology, Internal Medicine III, Medical University of Vienna, Vienna 1040, Austria
Author contributions: Tardelli M wrote, ideated, and proofread this manuscript.
Conflict-of-interest statement: There is no conflict of interest associated with any of the senior author or other coauthors contributed their efforts in this manuscript.
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: http://creativecommons.org/licenses/by-nc/4.0/
Corresponding author: Matteo Tardelli, MSc, PhD, Lecturer, Postdoctoral Fellow, Division of Gastroenterology and Hepatology, Joan and Sanford I Weill Department of Medicine, Weill Cornell Medical College, 413 E. 69th Street, New York, NY 10021, United States. mat4005@med.cornell.edu
Received: March 18, 2020
Peer-review started: March 18, 2020
First decision: May 15, 2020
Revised: June 18, 2020
Accepted: June 23, 2020
Article in press: June 23, 2020
Published online: July 7, 2020
Processing time: 110 Days and 22 Hours
Core Tip

Core tip: Monoacylglycerol lipase inhibition/modulation is yet unappreciated however attractive therapeutic concept to limit liver disease as fatty acids may drive hepatocyte injury, fibrogenesis and change immune cells phenotype.