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Clinical Medicine & Research
Volume 4, Number 1 : 42 -52
doi:10.3121/cmr.4.1.42
© 2006 Marshfield Clinic
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Review

Dysregulation of Cell Adhesion Proteins and Cardiac Arrhythmogenesis

Jifen Li, MD, PhD, Vickas V. Patel, MD, PhD and Glenn L. Radice, PhD

Jifen Li, MD, PhD, Center for Research on Reproduction and Women’s Health, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania
Vickas V. Patel, MD, PhD, Division of Cardiovascular Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania
Glenn L. Radice, PhD, Center for Research on Reproduction and Women’s Health, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania

Reprint Requests: Glenn L. Radice, PhD, Center for Research on Reproduction and Women’s Health, University of Pennsylvania, 1355 Biomedical Research Building II/III, 421 Curie Blvd., Philadelphia, PA 19104, Tel.: 215-898-0164, Fax: 215-573-5408, Email: radice{at}mail.med.upenn.edu

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.

Key Words: Arrhythmia • Cadherin • Connexin • Gap junction • Intercalated disc




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