Cardiomyocytes in the adult mammal retain little or none of their developmental capacity for hyperplastic growth. As a consequence of this differentiated, nonproliferative phenotype, cardiomyocyte loss due to injury or disease is irreversible. Therapeutic intervention in end-stage diseased hearts is currently limited to cardiac transplantation. An increase in cardiomyocyte number in diseased hearts could improve function. Augmentation of the cardiomyocyte population may be achievable by the expression of regulatory proteins in the myocardium, or by intracardiac grafting of exogenous cardiomyocytes.
|Original language||English (US)|
|Number of pages||9|
|Journal||Annals of the New York Academy of Sciences|
|State||Published - Mar 1995|
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)
- History and Philosophy of Science