Diabetic hyperglycaemia activates CaMKII and arrhythmias by O-linked glycosylation

Jeffrey R. Erickson, Laetitia Pereira, Lianguo Wang, Guanghui Han, Amanda Ferguson, Khanha Dao, Ronald J. Copeland, Florin Despa, Gerald W. Hart, Crystal M. Ripplinger and Donald M. Bers ()
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Jeffrey R. Erickson: University of California, Davis, 451 Health Sciences Drive, Davis, California 95616, USA
Laetitia Pereira: University of California, Davis, 451 Health Sciences Drive, Davis, California 95616, USA
Lianguo Wang: University of California, Davis, 451 Health Sciences Drive, Davis, California 95616, USA
Guanghui Han: Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, Maryland 21205, USA
Amanda Ferguson: University of California, Davis, 451 Health Sciences Drive, Davis, California 95616, USA
Khanha Dao: University of California, Davis, 451 Health Sciences Drive, Davis, California 95616, USA
Ronald J. Copeland: Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, Maryland 21205, USA
Florin Despa: University of California, Davis, 451 Health Sciences Drive, Davis, California 95616, USA
Gerald W. Hart: Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, Maryland 21205, USA
Crystal M. Ripplinger: University of California, Davis, 451 Health Sciences Drive, Davis, California 95616, USA
Donald M. Bers: University of California, Davis, 451 Health Sciences Drive, Davis, California 95616, USA

Nature, 2013, vol. 502, issue 7471, 372-376

Abstract: CaMKII is known to be pathologically activated in heart failure and arrhythmias; here it is shown that glucose-induced CaMKII activation via O-linked glycosylation might contribute to cardiac pathology in diabetes.

Date: 2013
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DOI: 10.1038/nature12537

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