 In a hamster model of cardiomyopathy and heart failure, cell-cell adhesions were irregular and disorganized, and expression levels of adherens junction/intercalated disc and nuclear pools of beta-catenin were decreased.These data suggest that a loss of beta-catenin may play a role in the diseased intercalated discs that have been associated with cardiac muscle hypertrophy and heart failure.In a rat model of myocardial infarction, adenoviral gene transfer of nonphosphorylatable, constitutively-active beta-catenin decreased MI size, activated the cell cycle, and reduced the amount of apoptosis in cardiomyocytes and cardiac myofibroblasts.