期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 20, 期 2, 页码 -出版社
MDPI
DOI: 10.3390/ijms20020404
关键词
ischemia-reperfusion injury; O-GlcNAc; cardioprotection
资金
- Fondation Leducq [CVD06]
- Danish Council for Strategic Research [11-108354]
- Novo Nordisk Foundation [NNF15OC0016674]
- Trygfonden [109624]
- British Heart Foundation [CS/14/3/31002]
- National Institute for Health Research
- University College London Hospitals Biomedical Research Centre
- Duke-National University Singapore Medical School
- Singapore Ministry of Health's National Medical Research Council under its Clinician Scientist-Senior Investigator scheme [NMRC/CSA-SI/0011/2017]
- Collaborative Centre Grant scheme [NMRC/CGAug16C006]
- COST Action EU-CARDIOPROTECTION [CA16225]
- COST (European Cooperation in Science and Technology)
Ischemia reperfusion injury (IR injury) associated with ischemic heart disease contributes significantly to morbidity and mortality. O-linked -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.
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