Basic Study
Copyright ©The Author(s) 2020. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Hepatol. Nov 27, 2020; 12(11): 931-948
Published online Nov 27, 2020. doi: 10.4254/wjh.v12.i11.931
Inhibition of vascular adhesion protein-1 modifies hepatic steatosis in vitro and in vivo
Emma L Shepherd, Sumera Karim, Philip N Newsome, Patricia F Lalor
Emma L Shepherd, Sumera Karim, Philip N Newsome, Patricia F Lalor, Centre for Liver and Gastroenterology Research, Birmingham National Institute for Health Research, Birmingham Biomedical Research Centre, Institute of Immunology and Immunotherapy, University of Birmingham, Birmingham B15 2TT, West Midlands, United Kingdom
Philip N Newsome, Liver Unit, Queen Elizabeth Hospital, University Hospitals Birmingham, Birmingham B15 2TT, West Midlands, United Kingdom
Author contributions: Shepherd EL, Karim S, Newsome PN and Lalor PF contributed to the writing and revising of the manuscript.
Institutional review board statement: The study was reviewed and approved by The Black Country Research Ethics Committee (06/Q702/61).
Institutional animal care and use committee statement: All mice were maintained and housed under conventional conditions in the Biomedical Services Unit at the University of Birmingham, United Kingdom. All animal experiments were performed under a Home Office project license in accordance with United Kingdom legislation and welfare guidelines, and studies were approved by the local ethical review board.
Conflict-of-interest statement: This study includes independent research supported by the Birmingham National Institute for Health Research (NIHR) Birmingham Biomedical Research Centre based at the University of Birmingham. The views expressed are those of the authors and not necessarily those of the NHS, the National Institute of Health Research or the Department of Health and Social Science. These studies were in part funded by a Biotechnology and Biosciences Research Council case studentship (BB/G529824/1) to P. F. Lalor for S. Karim. No other conflict of interest.
Data sharing statement: No additional data are available.
ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.
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: Patricia F Lalor, BSc, PhD, Academic Research, Reader (Associate Professor), Centre for Liver and Gastroenterology Research, Birmingham National Institute for Health Research, Birmingham Biomedical Research Centre, Institute of Immunology and Immunotherapy, University of Birmingham, Edgbaston, Birmingham B15 2TT, West Midlands, United Kingdom. p.f.lalor@bham.ac.uk
Received: June 15, 2020
Peer-review started: June 15, 2020
First decision: June 20, 2020
Revised: July 23, 2020
Accepted: September 15, 2020
Article in press: September 15, 2020
Published online: November 27, 2020
Processing time: 161 Days and 18.5 Hours
Core Tip

Core Tip: Incidence of non-alcoholic fatty liver disease (NAFLD) is dramatically increasing worldwide but to date there are no licenced therapies. The challenge remains management of the diverse pathophysiology from simple steatosis, through inflammation and fibrosis and the systemic complications of the metabolic syndrome. Vascular adhesion protein-1 (VAP-1) is an enzyme with proven contributions to systemic and hepatic glucose handling, inflammation and fibrosis. We now show an additional role in hepatic steatosis. Thus our important data suggests that targeting the semicarbazide sensitive amine oxidase capacity of VAP-1 may represent a useful adjunct to other therapeutic strategies in NAFLD.