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World J Gastroenterol. Jul 21, 2018; 24(27): 2984-2994
Published online Jul 21, 2018. doi: 10.3748/wjg.v24.i27.2984
Role of aldehyde dehydrogenase 2 in ischemia reperfusion injury: An update
Arnau Panisello-Roselló, Alexandre Lopez, Emma Folch-Puy, Teresa Carbonell, Anabela Rolo, Carlos Palmeira, René Adam, Marc Net, Joan Roselló-Catafau
Arnau Panisello-Roselló, Emma Folch-Puy, Joan Roselló-Catafau, Department of Experimental Pathology, Institute of Biomedical Research of Barcelona (IIBB)-CSIC, Barcelona 08036, Spain
Alexandre Lopez, René Adam, Centre Hepatobiliare, AP-HP Hôpital Paul Brousse, Villejuif 75008, France
Teresa Carbonell, Department of Physiology, Faculty of Biology, Universitat de Barcelona, Barcelona 08036, Spain
Anabela Rolo, Carlos Palmeira, Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra 3004-517, Portugal
Marc Net, Institute Georges Lopez, Lissieu 69380, France
Author contributions: All authors contributed equally to the writing of the manuscript and approved the final version.
Conflict-of-interest statement: The authors have no conflict of interests 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: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Joan Roselló-Catafau PhD, Adjunct Professor, Doctor, Department of Experimental Pathology, Institute of Biomedical Research of Barcelona (IIBB)-CSIC, C/Roselló 161, Barcelona 08036, Spain. jrcbam@iibb.csic.es
Telephone: +34-93-3638333 Fax: +34-93-3638301
Received: April 12, 2018
Peer-review started: April 12, 2018
First decision: May 21, 2018
Revised: June 28, 2018
Accepted: June 30, 2018
Article in press: June 30, 2018
Published online: July 21, 2018
Processing time: 98 Days and 21.8 Hours
Abstract

Aldehyde dehydrogenase 2 (ALDH2) is best known for its critical detoxifying role in liver alcohol metabolism. However, ALDH2 dysfunction is also involved in a wide range of human pathophysiological situations and is associated with complications such as cardiovascular diseases, diabetes mellitus, neurodegenerative diseases and aging. A growing body of research has shown that ALDH2 provides important protection against oxidative stress and the subsequent loading of toxic aldehydes such as 4-hydroxy-2-nonenal and adducts that occur in human diseases, including ischemia reperfusion injury (IRI). There is increasing evidence of its role in IRI pathophysiology in organs such as heart, brain, small intestine and kidney; however, surprisingly few studies have been carried out in the liver, where ALDH2 is found in abundance. This study reviews the role of ALDH2 in modulating the pathways involved in the pathophysiology of IRI associated with oxidative stress, autophagy and apoptosis. Special emphasis is placed on the role of ALDH2 in different organs, on therapeutic “preconditioning” strategies, and on the use of ALDH2 agonists such as Alda-1, which may become a useful therapeutic tool for preventing the deleterious effects of IRI in organ transplantation.

Keywords: Aldehyde dehydrogenase 2; 4-hydroxy-2-nonenal autophagy; Apoptosis; Ischemia reperfusion injury; Preconditioning

Core tip: Aldehyde dehydrogenase 2 (ALDH2) plays a crucial role not only in liver ethanol metabolism but also in diverse pathophysiological dysfunctions including cardiovascular diseases, stroke, diabetes, neuro-degenerative dysfunctions, and aging. Its involvement has recently been identified in ischemia reperfusion injury (IRI). The present study provides an updated review of the literature on the role of ALDH2 in ischemia-reperfusion injury and its activation in different organs (heart, brain, kidney, intestine, etc) focusing especially on its possible use as a potential therapeutic target for preventing IRI associated with organ transplantation.