Abstract

Connexin 43 hemichannels in myocardial ischemia and ventricular arrhythmia: new potential therapeutic targets Despite different treatment modalities, heart disease remains the leading cause of death worldwide. Connexins are proteins that form hemichannels and gap junctions. Gap junctions are responsible for the propagation of electrical and chemical signals between myocardial cells and cells of the specialized conduction system in order to synchronize the cardiac cycle and to provide an adequate pumping function of the heart. Gap junctions are normally open, while hemichannels are closed, but pathological circumstances may close gap junctions and open hemichannels, thereby perturbing cardiac homeostasis. Connexin 43 (Cx43) is the predominant connexin in the ventricles and Cx43 dysfunction is related to arrhythmia, sudden cardiac death and myocardial ischemia. Until recently, most therapeutic strategies targeting Cx43 were non-specific with many off-target effects. Newly developed peptides that interfere with the Cx43 channel function, are more specific and demonstrate new potential therapeutic possibilities for the treatment of myocardial ischemia and arrhythmia.

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