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Cardiovascular Research 2004 62(2):335-344; doi:10.1016/j.cardiores.2003.12.017
© 2004 by European Society of Cardiology
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Copyright © 2004, European Society of Cardiology

Connexin 43 and ischemic preconditioning

Rainer Schulz* and Gerd Heusch

Institut für Pathophysiologie, Zentrum für Innere Medizin, Universitätsklinikum Essen, Hufelandstraße 55, 45122, Essen, Germany

* Corresponding author. Tel.: +49-201-723-4521; fax: +49-201-723-4481. Email address: rainer_schulz{at}uni-essen.de

Connexin 43 (Cx43) is the essential protein to form hemichannels and gap junctions in the myocardium. The phosphorylation status of Cx43 which is regulated by a variety of protein kinases and phosphatases determines hemichannel and/or gap junction conductance and permeability. Gap junctions are involved in cell–cell coupling while hemichannels contribute to cardiomyocyte volume regulation. Cx43-formed channels are involved in ischemia/reperfusion injury, since blockade of a large portion of Cx43-formed channels attenuates ischemic hypercontracture, infarct development and post myocardial infarction remodeling. Ischemic preconditioning's protection also depends on functional Cx43-formed channels, since uncoupling of channels or genetic Cx43 deficiency abolishes infarct size reduction by ischemic preconditioning. The exact underlying mechanism(s) how Cx43 mediates protection remain to be established.

KEYWORDS Connexin; Ischemia; Reperfusion; Preconditioning

Time for primary review 26 days


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