Dysregulation of cell adhesion proteins and cardiac arrhythmogenesis.

Proper mechanical and electrical coupling of cardiomyocytes is crucial for normal propagation of the electrical impulse throughout the working myocardium. Various proteins on the surface of cardiomyocytes are responsible for the integration of structural information and cell-cell communication. Increasing evidence from diseased myocardium and animal models indicates that alteration in electrical coupling via gap junctions is a critical determinant in the development of an arrhythmogenic substrate. What is less clear is how gap junctions are maintained and regulated in the working myocardium. In this review, we present data from human disease and animal models that support the idea that cell adhesion proteins regulate the stability of the gap junction protein, connexin.