Editorial

Cardiomyocyte replacement has been the focus of intense research because of the significant burden of heart fail-ure. Although the adult mammalian heart is nonregenera-tive, recent studies have demonstrated that it retains a modest degree of cardiomyocyte turnover throughout life, mediated primarily by the proliferation of preexisting cardiomyo-cytes.1,2 In contrast to the adult heart, the neonatal mamma-lian heart possesses a remarkable regenerative ability in the first few days of life mediated by the proliferation of preex-isting cardiomyocytes, after which cardiomyocytes perma-nently exit the cell cycle, and the regenerative ability of the heart is lost.3,4 Importantly, the embryonic mammalian heart also possesses a remarkable regenerative ability. Embryonic cardiomyocyte replacement studies were previously reported by the Cox5 and Torres6 groups. The Cox group showed that compensatory growth of cardiomyocytes occurred followin