Editorials |
From the Division of Cardiology, Johns Hopkins University.
Correspondence to Eduardo Marbán, Johns Hopkins University Division of Cardiology, 858 Ross Building, Baltimore, MD 21205. E-Mail marban@jhmi.edu
See related article, pages 536544
Key Words: stem cell electrophysiology calcium
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
As of August 2003, the prevailing dogma posited that the heart is a terminally-differentiated organ, that the myocytes we have now are those we were born with (only bigger), and that the best hope for treating cardiac injury is to limit the insult (eg, by prompt reperfusion) or to block secondary maladaptive pathways. Because of pioneering work from various laboratories,13 the concept of cardiac plasticity has come to replace the old static-organ dogma. We now believe that the normal adult heart is the net result of a slow rate of cell loss balanced by ongoing cell replacement. The predominant mode of cell loss is via apoptosis, reflecting the normal processes of wear and tear. Cell replacement, on the other hand, taps into a reservoir of resident cardiac stem cells (CSCs). Such CSCs lurk in niches distributed inhomogeneously throughout the heart,4 and, when activated, enter the mitotic cycle to eventually become cardiomyocytes and vascular cells. Back-of-the-envelope calculations, based on the observed frequencies of apoptotic events and mitotic figure in heart tissue, lead us to estimate that cardiac myocytes turn over several times in a typical mammalian lifespan. While lamenting our complacency (how could we have missed [or dismissed] the evidence supporting turnover for so long?), it is important to recognize that the processes are slow and, statistically speaking, rare: CSCs comprise only 1 of 30 000 cells in the heart.1 On a more positive note, it is wondrous to observe how thoroughly the landscape has been transformed in less than four
Related Article:
Circ. Res. 2007 100: 536-544.
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