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lüll The role of protein O-linked beta-N-acetylglucosamine in mediating cardiac stress responses Chatham JC; Marchase RBBiochim Biophys Acta 2010[Feb]; 1800 (2): 57-66The modification of serine and threonine residues of nuclear and cytoplasmic proteins by O-linked beta-N-acetylglucosamine (O-GlcNAc) has emerged as a highly dynamic post-translational modification that plays a critical role in regulating numerous biological processes. Much of our understanding of the mechanisms underlying the role of O-GlcNAc on cellular function has been in the context of its adverse effects in mediating a range of chronic disease processes, including diabetes, cancer and neurodegenerative diseases. However, at the cellular level it has been shown that O-GlcNAc levels are increased in response to stress; augmentation of this response improved cell survival while attenuation decreased cell viability. Thus, it has become apparent that strategies that augment O-GlcNAc levels are pro-survival, whereas those that reduce O-GlcNAc levels decrease cell survival. There is a long history demonstrating the effectiveness of acute glucose-insulin-potassium (GIK) treatment and to a lesser extent glutamine in protecting against a range of stresses, including myocardial ischemia. A common feature of these approaches for metabolic cardioprotection is that they both have the potential to stimulate O-GlcNAc synthesis. Consequently, here we examine the links between metabolic cardioprotection with the ischemic cardioprotection associated with acute increases in O-GlcNAc levels. Some of the protective mechanisms associated with activation of O-GlcNAcylation appear to be transcriptionally mediated; however, there is also strong evidence to suggest that transcriptionally independent mechanisms also play a critical role. In this context we discuss the potential link between O-GlcNAcylation and cardiomyocyte calcium homeostasis including the role of non-voltage gated, capacitative calcium entry as a potential mechanism contributing to this protection.|Acetylglucosamine/*physiology[MESH]|Animals[MESH]|Calcium Channels/physiology[MESH]|Calcium/metabolism[MESH]|Cardiotonic Agents/*metabolism[MESH]|Glucose/metabolism[MESH]|Glutamine/metabolism[MESH]|Hexosamines/biosynthesis[MESH]|Homeostasis/physiology[MESH]|Humans[MESH]|In Vitro Techniques[MESH]|Membrane Proteins/physiology[MESH]|Myocardial Reperfusion Injury/physiopathology[MESH]|Myocytes, Cardiac/metabolism[MESH]|Neoplasm Proteins/physiology[MESH]|ORAI1 Protein[MESH]|Protein Processing, Post-Translational[MESH]|Proteins/metabolism[MESH]|Stress, Physiological/*physiology[MESH]|Stromal Interaction Molecule 1[MESH] |