Copyright ©The Author(s) 2018. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Aug 21, 2018; 24(31): 3521-3530
Published online Aug 21, 2018. doi: 10.3748/wjg.v24.i31.3521
Ubiquitin-proteasome system and oxidative stress in liver transplantation
Norma Alva, Arnau Panisello-Roselló, Marta Flores, Joan Roselló-Catafau, Teresa Carbonell
Norma Alva, Marta Flores, Teresa Carbonell, Department of Cell Biology, Physiology and Immunology, University of Barcelona, Barcelona 08028, Spain
Arnau Panisello-Roselló, Joan Roselló-Catafau, Experimental Pathology Department, Institute of Biomedical Research of Barcelona, Barcelona 08036, Spain
Author contributions: All authors contribute equally to the writing of the manuscript and approved the final version.
Supported by Fondo de Investigaciones Sanitarias, Ministerio de Economia y Competitividad (Madrid, Spain), No. PI15/00110.
Conflict-of-interest statement: The authors have no conflict of interest to declare.
Open-Access: 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:
Correspondence to: Teresa Carbonell, PhD, Associate Professor, Research Scientist, Department of Cell Biology, Physiology and Immunology, University of Barcelona, Avda Diagonal, 643, Barcelona 08028, Catalonia, Spain.
Telephone: +34-93-4035924
Received: May 5, 2018
Peer-review started: May 5, 2018
First decision: May 17, 2018
Revised: June 28, 2018
Accepted: June 30, 2018
Article in press: June 30, 2018
Published online: August 21, 2018

A major issue in organ transplantation is the development of a protocol that can preserve organs under optimal conditions. Damage to organs is commonly a consequence of flow deprivation and oxygen starvation following the restoration of blood flow and reoxygenation. This is known as ischemia-reperfusion injury (IRI): a complex multifactorial process that causes cell damage. While the oxygen deprivation due to ischemia depletes cell energy, subsequent tissue oxygenation due to reperfusion induces many cascades, from reactive oxygen species production to apoptosis initiation. Autophagy has also been identified in the pathogenesis of IRI, although such alterations and their subsequent functional significance are controversial. Moreover, proteasome activation may be a relevant pathophysiological mechanism. Different strategies have been adopted to limit IRI damage, including the supplementation of commercial preservation media with pharmacological agents or additives. In this review, we focus on novel strategies related to the ubiquitin proteasome system and oxidative stress inhibition, which have been used to minimize damage in liver transplantation.

Keywords: Liver transplant, Ischemia-reperfusion injury, Oxidative stress, Proteasome, Redox regulation, Ubiquitin

Core tip: Ischemia-reperfusion injury is a complex multifactorial process that causes cell damage during liver transplantation. The role of the ubiquitin proteasome system during liver transplantation remains unclear. The use of proteasome inhibitors is a new strategy aimed at improving organ preservation.