Ubiquitin-proteasome system and oxidative stress in liver transplantation
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-reperfu...
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Published in: | World journal of gastroenterology : WJG Vol. 24; no. 31; pp. 3521 - 3530 |
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Main Authors: | , , , , |
Format: | Journal Article |
Language: | English |
Published: |
United States
Baishideng Publishing Group
21-08-2018
Baishideng Publishing Group Inc |
Subjects: | |
Online Access: | Get full text |
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Summary: | 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. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 Author contributions: All authors contribute equally to the writing of the manuscript and approved the final version. Telephone: +34-93-4035924 Supported by Fondo de Investigaciones Sanitarias, Ministerio de Economia y Competitividad (Madrid, Spain), No. PI15/00110. 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. tcarbonell@ub.edu |
ISSN: | 1007-9327 2219-2840 |
DOI: | 10.3748/wjg.v24.i31.3521 |