The post-translational modification of serine and threonine residues of proteins found in numerous subcellular locations by O-linked N-acetylglucosamine (O-GlcNAc) is emerging as a key mediator of many cardiovascular pathophysiological processes. Early studies implicated increased protein O-GlcNAcylation as contributing to the cardiovascular complications associated with diabetes, whereas subsequent studies demonstrated that acute increases in O-GlcNAc levels were protective against ischemia/reperfusion injury. There is now a growing understanding that O-GlcNAc modification of proteins influences numerous cellular functions, including transcription, protein turnover, calcium handling, and bioenergetics. As a result, a more nuanced view of the role of protein O-GlcNAcylation in the cardiovascular system is emerging along with the recognition that it is required for normal cellular function and homeostasis. Consequently, the impact of changes in O-GlcNAc cycling due to stress or disease on the heart is complex and highly dependent on the specific context of these events. The goal of this review is to provide an overview of some of the more recent advances in our understanding of the role O-GlcNAcylation plays in mediating cardiovascular function and disease.
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April 2017
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This artistic rendition shows an Atomic Force Microscopy tip probing the mechanics of an individual virus particle. The colour scale of the particle indicates the deformation and stress of the viral shell obtained with Finite Element Analysis. The applied force is monitored by focusing a laser beam at the end of the microcantilever. For more information please see study by Moreno-Madrid et al. in this issue, pages 499–511. Image provided by Pedro De Pablo.
Review Article|
April 13 2017
O-GlcNAcylation and cardiovascular disease
JaLessa N. Wright;
JaLessa N. Wright
1Division of Molecular and Cellular Pathology, Department of Pathology, University of Alabama at Birmingham, Birmingham, AL, U.S.A.
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Helen E. Collins;
Helen E. Collins
1Division of Molecular and Cellular Pathology, Department of Pathology, University of Alabama at Birmingham, Birmingham, AL, U.S.A.
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Adam R. Wende;
Adam R. Wende
1Division of Molecular and Cellular Pathology, Department of Pathology, University of Alabama at Birmingham, Birmingham, AL, U.S.A.
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John C. Chatham
1Division of Molecular and Cellular Pathology, Department of Pathology, University of Alabama at Birmingham, Birmingham, AL, U.S.A.
Correspondence: John C. Chatham (jchatham@uabmc.edu)
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Publisher: Portland Press Ltd
Received:
November 29 2016
Revision Received:
February 13 2017
Accepted:
February 16 2017
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© 2017 The Author(s); published by Portland Press Limited on behalf of the Biochemical Society
2017
Biochem Soc Trans (2017) 45 (2): 545–553.
Article history
Received:
November 29 2016
Revision Received:
February 13 2017
Accepted:
February 16 2017
Citation
JaLessa N. Wright, Helen E. Collins, Adam R. Wende, John C. Chatham; O-GlcNAcylation and cardiovascular disease. Biochem Soc Trans 15 April 2017; 45 (2): 545–553. doi: https://doi.org/10.1042/BST20160164
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