Copyright
©The Author(s) 2022. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Clin Cases. Apr 26, 2022; 10(12): 3662-3676
Published online Apr 26, 2022. doi: 10.12998/wjcc.v10.i12.3662
Published online Apr 26, 2022. doi: 10.12998/wjcc.v10.i12.3662
Pathophysiological mechanisms of hepatic stellate cells activation in liver fibrosis
Dmitry Victorovich Garbuzenko, Department of Faculty Surgery, South Ural State Medical University, Chelyabinsk 454092, Russia
Author contributions: Garbuzenko DV contributed to the conception, design, acquisition, analysis, interpretation of data, wrote the manuscript and approved the final version.
Conflict-of-interest statement: All authors have no conflicts of interest to declare.
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: Dmitry Victorovich Garbuzenko, MD, PhD, DSc (Med), Professor, Department of Faculty Surgery, South Ural State Medical University, PO Box 12317, Chelyabinsk 454080, Russia. garb@inbox.ru
Received: July 27, 2021
Peer-review started: July 27, 2021
First decision: October 3, 2021
Revised: October 17, 2021
Accepted: March 25, 2022
Article in press: March 25, 2022
Published online: April 26, 2022
Processing time: 268 Days and 5.4 Hours
Peer-review started: July 27, 2021
First decision: October 3, 2021
Revised: October 17, 2021
Accepted: March 25, 2022
Article in press: March 25, 2022
Published online: April 26, 2022
Processing time: 268 Days and 5.4 Hours
Core Tip
Core tip: This review focuses on the pathophysiological mechanisms of hepatic stellate cells activation in liver fibrosis. A better understanding of these pathophysiological mechanisms gave rise to drugs preventing liver fibrosis development and progression. In this respect, the disorder of the intracellular signaling regulation, epigenetic changes, and cellular stress response can be the target of an action aimed at hepatic stellate cells deactivation. This can be achieved by inducing their return to an inactive state, cellular aging, apoptosis, and/or clearance by immune cells, and may serve as potential antifibrotic therapy.