Key result
Cell adhesion proteins regulate the stability of the gap junction protein, connexin, which is a critical determinant in the development of an arrhythmogenic substrate.
This review highlights the mechanistic role of cell adhesion proteins in regulating gap junction stability and their contribution to cardiac arrhythmogenesis.
Gap junction alterations may promote arrhythmogenesis; leaves open whether targeting them improves patient outcomes.
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.
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Li et al. (2006) conducted a review in Cardiac Arrhythmogenesis. Cell adhesion proteins was evaluated. Cell adhesion proteins regulate the stability of the gap junction protein, connexin, which is a critical determinant in the development of an arrhythmogenic substrate.
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