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CyclinD2-overexpression augment the afterload induced hypertrophic response and improves the survival
No full textCell Cycle-Mediated Cardiac Regeneration in the Mouse Heart
No full textMany forms of heart disease result in the essentially irreversible loss of cardiomyocytes. The ability to promote cardiomyocyte renewal may be a promising approach to reverse injury in diseased hearts. PURPOSE OF REVIEW: To describe the impact of cardiomyocyte cell cycle activation on cardiac function and structure in several different models of myocardial disease. RECENT FINDINGS: Transgenic mice expressing cyclin D2 (D2 mice) exhibit sustained cardiomyocyte renewal in the adult heart. Earlier studies demonstrated that D2 mice exhibited progressive myocardial regeneration in experimental models of myocardial infarction, and that cardiac function was normalized to values seen in sham operated litter mates by 180 days post-injury. D2 mice also exhibited markedly improved atrial structure in a genetic model of atrial fibrosis. More recent studies revealed that D2 mice were remarkably resistant to heart failure induced by chronic elevated afterload as compared to their wild type (WT siblings), with a 6-fold increase in median survival as well as retention of relatively normal cardiac function. Finally, D2 mice exhibited a progressive recovery in cardiac function to normal levels and a concomitant reduction in adverse myocardial remodeling in an anthracycline cardiotoxicity model. SUMMARY: The studies reviewed here make a strong case for the potential utility of inducing cardiomyocyte renewal as a means to treat injured hearts. Several challenges which must be met to develop a viable therapeutic intervention based on these observations are discussed
CyclinD2-overexpression augment the afterload induced hypertrophic response and improves the survival
No full text
Afterload but not preload induces proliferation of cardiomyocytes and improves survival in cyclinD2-overexpressing mice
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Cardiomyocte cell cycle induction improves the survival in pressure overload induced heart failure
No full textAfterload but not preload induces proliferation of cardiomyocytes and improves survival in cyclinD2-overexpressing mice
No full textCardiomyocte cell cycle induction improves the survival in pressure overload induced heart failure
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