Volume 233, Issue 1 e13696
REVIEW ARTICLE

Protein O-GlcNAcylation in the heart

Yann Huey Ng

Yann Huey Ng

Department of Medicine and HeartOtago, University of Otago, Dunedin, New Zealand

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Chidinma A. Okolo

Chidinma A. Okolo

Department of Physiology and HeartOtago, University of Otago, Dunedin, New Zealand

Life Sciences Division, Diamond Light Source Ltd, Harwell Science and Innovation Campus, Didcot, UK

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Jeffrey R. Erickson

Jeffrey R. Erickson

Department of Physiology and HeartOtago, University of Otago, Dunedin, New Zealand

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James C. Baldi

James C. Baldi

Department of Medicine and HeartOtago, University of Otago, Dunedin, New Zealand

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Peter P. Jones

Corresponding Author

Peter P. Jones

Department of Physiology and HeartOtago, University of Otago, Dunedin, New Zealand

Correspondence

Peter P. Jones, Department of Physiology and HeartOtago, School of Biomedical Sciences, University of Otago, 270 Great King Street, Dunedin Central, Dunedin 9016, New Zealand.

Email: [email protected]

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First published: 31 May 2021
Citations: 10

Yann Huey Ng and Chidinma A. Okolo contributed equally to this manuscript.

Abstract

O-GlcNAcylation is a ubiquitous post-translational modification that is extremely labile and plays a significant role in physiology, including the heart. Sustained activation of cardiac O-GlcNAcylation is frequently associated with alterations in cellular metabolism, leading to detrimental effects on cardiovascular function. This is particularly true during conditions such as diabetes, hypertension, cardiac remodelling, heart failure and arrhythmogenesis. Paradoxically, transient elevation of cardiac protein O-GlcNAcylation can also exert beneficial effects in the heart. There is compelling evidence to suggest that a complex interaction between O-GlcNAcylation and phosphorylation also exists in the heart. Beyond direct functional consequences on cardiomyocytes, O-GlcNAcylation also acts indirectly by altering the function of transcription factors that affect downstream signalling. This review focuses on the potential cardioprotective role of protein O-GlcNAcylation during ischaemia-reperfusion injury, the deleterious consequences of chronically elevated O-GlcNAc levels, the interplay between O-GlcNAcylation and phosphorylation in the cardiomyocytes and the effects of O-GlcNAcylation on other major non-myocyte cell types in the heart.

CONFLICT OF INTEREST

The authors have declared no conflict of interest.

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