Petagine L, Zariwala MG, Patel VB. Alcoholic liver disease: Current insights into cellular mechanisms. World J Biol Chem 2021; 12(5): 87-103 [PMID: 34630912 DOI: 10.4331/wjbc.v12.i5.87]
Corresponding Author of This Article
Vinood B Patel, FRSC, PhD, Reader (Associate Professor), Center for Nutraceuticals, School of Life Sciences, University of Westminster, 115 New Cavendish Street, London W1W 6UW, United Kingdom. v.b.patel@westminster.ac.uk
Research Domain of This Article
Pathology
Article-Type of This Article
Review
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 Biol Chem. Sep 27, 2021; 12(5): 87-103 Published online Sep 27, 2021. doi: 10.4331/wjbc.v12.i5.87
Alcoholic liver disease: Current insights into cellular mechanisms
Lucy Petagine, Mohammed Gulrez Zariwala, Vinood B Patel
Lucy Petagine, Mohammed Gulrez Zariwala, Vinood B Patel, Center for Nutraceuticals, School of Life Sciences, University of Westminster, London W1W 6UW, United Kingdom
Author contributions: Petagine L performed the literature search, wrote the original draft, designed the figures; Petagine L, Patel VB and Zariwala MG reviewed and edited the final manuscript; all authors have read and agreed to the published version of the manuscript.
Conflict-of-interest statement: There is no conflict of interest.
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: Vinood B Patel, FRSC, PhD, Reader (Associate Professor), Center for Nutraceuticals, School of Life Sciences, University of Westminster, 115 New Cavendish Street, London W1W 6UW, United Kingdom. v.b.patel@westminster.ac.uk
Received: April 30, 2021 Peer-review started: April 30, 2021 First decision: July 8, 2021 Revised: July 20, 2021 Accepted: August 12, 2021 Article in press: August 12, 2021 Published online: September 27, 2021 Processing time: 144 Days and 22.3 Hours
Abstract
Alcoholic liver disease (ALD) due to chronic alcohol consumption is a significant global disease burden and a leading cause of mortality. Alcohol abuse induces a myriad of aberrant changes in hepatocytes at both the cellular and molecular level. Although the disease spectrum of ALD is widely recognized, the precise triggers for disease progression are still to be fully elucidated. Oxidative stress, mitochondrial dysfunction, gut dysbiosis and altered immune system response plays an important role in disease pathogenesis, triggering the activation of inflammatory pathways and apoptosis. Despite many recent clinical studies treatment options for ALD are limited, especially at the alcoholic hepatitis stage. We have therefore reviewed some of the key pathways involved in the pathogenesis of ALD and highlighted current trials for treating patients.
Core Tip: Alcoholic liver disease (ALD) causes significant global disease burden inducing both cellular and molecular modifications in hepatocytes. Although the spectrum of disease is widely recognized, the precise disease pathogenesis is yet to be fully elucidated. In this review we summarize some of the key pathways responsible for the pathogenesis of ALD and highlight current available treatments.
