Volume 69 Number 6 November 2002	back to contents

From the Section of Myocardial Biology, Cardiovascular Institute and Department of Medicine, Mount Sinai School of Medicine, New York, NY.

Address correspondence to David E. Gutstein, M.D., Box 1030, Mount Sinai School of Medicine, One East 100th Street, New York, NY 10029.

Adapted from a presentation given at Grand Rounds of the Cardiovascular Institute, Mount Sinai School of Medicine, New York, NY on October 15, 2001, and updated on February 19, 2002.

ABSTRACT

Cardiac gap junctions have been implicated in maintaining cardiac conduction and function. In cardiac disease, expression of connexin43, the most abundant ventricular gap junction protein, is markedly abnormal, a process termed “gap junction remodeling.” To date, however, the gap junction has not been directly targeted therapeutically in cardiac disease states. Therefore, we have developed novel and complementary experimental models to investigate whether loss of connexin43 expression in the heart can be directly linked to the arrhythmic and functional complications of heart disease. In this article, we discuss how data from connexin43 conditional and chimeric knock-out mice support the hypothesis that gap junction remodeling is a key molecular feature underlying the high incidence of sudden arrhythmic death and exacerbating the ventricular dysfunction associated with acquired heart disease.

KEYWORDS

Gap junction, connexin43, arrhythmia, heart

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