Please use this identifier to cite or link to this item: https://doi.org/10.3390/ijms20020404
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dc.titleThe role of O-GlcNAcylation for protection against ischemia-reperfusion injury
dc.contributor.authorJensen, R.V
dc.contributor.authorAndreadou, I
dc.contributor.authorHausenloy, D.J
dc.contributor.authorBøtker, H.E
dc.date.accessioned2020-11-10T00:47:23Z
dc.date.available2020-11-10T00:47:23Z
dc.date.issued2019
dc.identifier.citationJensen, 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
dc.identifier.issn16616596
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/183292
dc.description.abstractIschemia 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.
dc.rightsAttribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.sourceUnpaywall 20201031
dc.subjectcalcium
dc.subjectmitochondrial permeability transition pore
dc.subjectn acetylglucosamine
dc.subjectcardiotonic agent
dc.subjectcarrier protein
dc.subjectn acetylglucosamine
dc.subjectreactive oxygen metabolite
dc.subjectbiosynthesis
dc.subjectcell death
dc.subjectcell survival
dc.subjectcell viability
dc.subjectdiabetes mellitus
dc.subjectendoplasmic reticulum stress
dc.subjectfluorescence microscopy
dc.subjectgene overexpression
dc.subjectheart function
dc.subjectheart protection
dc.subjectheat shock response
dc.subjecthemodynamics
dc.subjecthuman
dc.subjectinflammation
dc.subjectischemic heart disease
dc.subjectischemic preconditioning
dc.subjectmorbidity
dc.subjectmortality
dc.subjectnonhuman
dc.subjectoxidative stress
dc.subjectreperfusion injury
dc.subjectReview
dc.subjectsignal transduction
dc.subjectstress
dc.subjectanimal
dc.subjectcomorbidity
dc.subjectdrug effect
dc.subjectmetabolism
dc.subjectmyocardial ischemia reperfusion injury
dc.subjectoxidative stress
dc.subjectpathology
dc.subjectprotein processing
dc.subjectreperfusion injury
dc.subjectAcetylglucosamine
dc.subjectAnimals
dc.subjectCardiotonic Agents
dc.subjectComorbidity
dc.subjectHumans
dc.subjectMetabolic Networks and Pathways
dc.subjectMitochondrial Membrane Transport Proteins
dc.subjectMyocardial Reperfusion Injury
dc.subjectOxidative Stress
dc.subjectProtein Processing, Post-Translational
dc.subjectReactive Oxygen Species
dc.subjectReperfusion Injury
dc.typeReview
dc.contributor.departmentDUKE-NUS MEDICAL SCHOOL
dc.description.doi10.3390/ijms20020404
dc.description.sourcetitleInternational Journal of Molecular Sciences
dc.description.volume20
dc.description.issue2
dc.description.page404
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