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 arrythmic death and exacerbating the ventricular dysfunction associated with acquired heart disease.
|Number of pages||4|
|Journal||Mount Sinai Journal of Medicine|
|State||Published - Nov 2002|
- Gap junction