Journal
CELLULAR SIGNALLING
Volume 86, Issue -, Pages -Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.cellsig.2021.110070
Keywords
Protein phosphatase; Connexin 43; Dephosphorylation; PP1; PP2A; Calcineurin
Categories
Funding
- National Institutes of Health [R01-AA024769, R01-HL113640, R01-HL146744, HL80101]
- American Heart Association [25860028]
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This review focuses on the regulation of Cx43 phosphorylation state and cell-to-cell communication by serine-threonine protein phosphatases, and their impact on arrhythmogenesis in chronic heart failure, myocardial ischemia, and atrial fibrillation. The therapeutic potential of modulating protein phosphatases to treat arrhythmias in these clinical settings is also discussed.
Regulation of cell-to-cell communication in the heart by the gap junction protein Connexin43 (Cx43) involves modulation of Cx43 phosphorylation state by protein kinases, and dephosphorylation by protein phosphatases. Dephosphorylation of Cx43 has been associated with impaired intercellular coupling and enhanced arrhythmogenesis in various pathologic states. While there has been extensive study of the protein kinases acting on Cx43, there has been limited studies of the protein phosphatases that may underlie Cx43 dephosphorylation. The focus of this review is to introduce serine-threonine protein phosphatase regulation of Cx43 phosphorylation state and cell-to-cell communication, and its impact on arrhythmogenesis in the setting of chronic heart failure and myocardial ischemia, as well as on atrial fibrillation. We also discuss the therapeutic potential of modulating protein phosphatases to treat arrhythmias in these clinical settings.
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