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The Role of O-GlcNAcylation for Protection against Ischemia-Reperfusion Injury

1
Department of Cardiology, Aarhus University Hospital, Skejby, Palle Juul-Jensens Blvd. 99, 8200 Aarhus N, Denmark
2
Laboratory of Pharmacology, Faculty of Pharmacy, National and Kapodistrian University of Athens Panepistimiopolis, 15771 Zografou, Greece
3
Cardiovascular & Metabolic Disorders Program, Duke-National University of Singapore Medical School, Singapore 169857, Singapore
4
National Heart Research Institute Singapore, National Heart Centre, Singapore 169609, Singapore
5
Yong Loo Lin School of Medicine, National University Singapore, Singapore 119228, Singapore
6
The Hatter Cardiovascular Institute, University College London, London WC1E 6HX, UK
7
The National Institute of Health Research University College London Hospitals Biomedical Research Centre, Research & Development, London W1T 7DN, UK
8
Tecnologico de Monterrey, Centro de Biotecnologia-FEMSA, Monterrey 64849, Mexico
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2019, 20(2), 404; https://doi.org/10.3390/ijms20020404
Received: 30 November 2018 / Revised: 12 January 2019 / Accepted: 15 January 2019 / Published: 18 January 2019
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Abstract

Ischemia reperfusion injury (IR injury) associated with ischemic heart disease contributes significantly to morbidity and mortality. O-linked β-N-acetylglucosamine (O-GlcNAc) is a dynamic posttranslational modification that plays an important role in numerous biological processes, both in normal cell functions and disease. O-GlcNAc increases in response to stress. This increase mediates stress tolerance and cell survival, and is protective. Increasing O-GlcNAc is protective against IR injury. Experimental cellular and animal models, and also human studies, have demonstrated that protection against IR injury by ischemic preconditioning, and the more clinically applicable remote ischemic preconditioning, is associated with increases in O-GlcNAc levels. In this review we discuss how the principal mechanisms underlying tissue protection against IR injury and the associated immediate elevation of O-GlcNAc may involve attenuation of calcium overload, attenuation of mitochondrial permeability transition pore opening, reduction of endoplasmic reticulum stress, modification of inflammatory and heat shock responses, and interference with established cardioprotective pathways. O-GlcNAcylation seems to be an inherent adaptive cytoprotective response to IR injury that is activated by mechanical conditioning strategies. View Full-Text
Keywords: ischemia-reperfusion injury; O-GlcNAc; cardioprotection ischemia-reperfusion injury; O-GlcNAc; cardioprotection
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Jensen, R.V.; Andreadou, I.; Hausenloy, D.J.; Bøtker, H.E. The Role of O-GlcNAcylation for Protection against Ischemia-Reperfusion Injury. Int. J. Mol. Sci. 2019, 20, 404.

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