Please use this identifier to cite or link to this item: https://doi.org/10.3390/ijms20020404
Title: The role of O-GlcNAcylation for protection against ischemia-reperfusion injury
Authors: Jensen, R.V
Andreadou, I
Hausenloy, D.J 
Bøtker, H.E
Keywords: calcium
mitochondrial permeability transition pore
n acetylglucosamine
cardiotonic agent
carrier protein
n acetylglucosamine
reactive oxygen metabolite
biosynthesis
cell death
cell survival
cell viability
diabetes mellitus
endoplasmic reticulum stress
fluorescence microscopy
gene overexpression
heart function
heart protection
heat shock response
hemodynamics
human
inflammation
ischemic heart disease
ischemic preconditioning
morbidity
mortality
nonhuman
oxidative stress
reperfusion injury
Review
signal transduction
stress
animal
comorbidity
drug effect
metabolism
myocardial ischemia reperfusion injury
oxidative stress
pathology
protein processing
reperfusion injury
Acetylglucosamine
Animals
Cardiotonic Agents
Comorbidity
Humans
Metabolic Networks and Pathways
Mitochondrial Membrane Transport Proteins
Myocardial Reperfusion Injury
Oxidative Stress
Protein Processing, Post-Translational
Reactive Oxygen Species
Reperfusion Injury
Issue Date: 2019
Citation: Jensen, R.V, Andreadou, I, Hausenloy, D.J, Bøtker, H.E (2019). The role of O-GlcNAcylation for protection against ischemia-reperfusion injury. International Journal of Molecular Sciences 20 (2) : 404. ScholarBank@NUS Repository. https://doi.org/10.3390/ijms20020404
Rights: Attribution 4.0 International
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. © 2019 by the authors. Licensee MDPI, Basel, Switzerland.
Source Title: International Journal of Molecular Sciences
URI: https://scholarbank.nus.edu.sg/handle/10635/183292
ISSN: 16616596
DOI: 10.3390/ijms20020404
Rights: Attribution 4.0 International
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