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Cardiovascular Research 2004 61(3):386-401; doi:10.1016/j.cardiores.2003.11.039
© 2004 by European Society of Cardiology
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Copyright © 2003, European Society of Cardiology

Gap junction-mediated spread of cell injury and death during myocardial ischemia–reperfusion

David García-Dorado*, Antonio Rodríguez-Sinovas and Marisol Ruiz-Meana

Laboratorio de Cardiología Experimental, Servicio de Cardiología, Hospital Universitario Valle de Hebron, Barcelona, Spain

* Corresponding author. Laboratorio de Investigación Cardiovascular, Hospitals Vall d'Hebron, Pg. Vall d'Hebron 119–129, 08035 Barcelona, Spain. Tel.: +34-93-4894038; fax: +34-93-4894032. dgdorado{at}vhebron.net

Gap junction-mediated intercellular communication (GJMIC) has been known for a long time to be essential in propagation of electrical impulse in the heart, and the contribution of altered GJMIC to the genesis of arrhythmias has been extensively investigated. However, although it is well known that GJMIC allows the exchange of biologically important molecules between adjacent cells, the pathophysiological significance of such chemical coupling during myocardial ischemia and reperfusion is much less known. It has been solidly established that ischemia impairs GJMIC and eventually leads to electrical uncoupling, but recent studies suggest that GJMIC may still allow synchronization of the onset of ischemic rigor contracture and of the progression of ischemic injury beyond rigor onset. During reperfusion, GJMIC has been shown to mediate cell-to-cell propagation of hypercontracture and cell death, and there is evidence that this phenomenon explains the continuity of areas of contraction band necrosis and contributes to final infarct size. Finally, there is increasing evidence that GJ or their protein components are involved in the genesis of the protective effect of ischemic preconditioning, although probably through mechanisms independent from modulator of GJMIC. GJ play an important role in the pathphysiology of cell injury and death during myocardial ischemia–reperfusion and are potential targets for new cardioprotective therapeutic strategies.

KEYWORDS Myocardial infarction; Ischemic heart disease; Cardiomyocytes

Time for primary review 9 days


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