| Popis: |
Ventricular myocytes of the adult mammalian myocardium are considered essentially incapable of regeneration. These cells cease dividing soon after birth and subsequent cardiac growth is brought about by increases in cellular size (hypertrophy) rather than cell number [1]. Following irreversible injury and death of cardiomyocytes, caused by a variety of factors such as ischemia, excess catecholamines or genetic defects, necrotic muscle becomes replaced by scar tissue. The remaining myocardium hypertrophies to meet the need for extra work but beyond a certain potential for adaptation, cardiac failure ensues. There is some evidence that ventricular myocytes may not have lost their proliferative potential irreversibly, since they can be stimulated to synthesize DNA in culture [2] and are apparently capable of a hyperplastic response in hypertrophie or ageing hearts [3]. |
