Abstract

The rationale for gene transfer of adenylyl cyclase type VI (AC(VI)) for clinical congestive heart failure (CHF) is based on recent experimental studies that have extended from cultured cardiac myocytes to preclinical studies in animal models of CHF. Over the past several years substantial data have indicated an unexpected and pronounced favorable effect of AC(VI) expression in cardiovascular disease. Preclinical studies have shown that increased cardiac AC content improves left ventricular function and attenuates deleterious remodeling in the failing heart, and reduces mortality in heart failure and in acute myocardial infarction. A brief review of the preclinical studies that have examined changes associated with increased AC expression in the heart is presented here.

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