Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation Research
Search: search_blue_button Advanced Search
Circulation Research. 2007;100:445-446
doi: 10.1161/01.RES.0000260271.33215.9b
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Marbán, E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Marbán, E.
Related Collections
Right arrowRelated Article
(Circulation Research. 2007;100:445.)
© 2007 American Heart Association, Inc.


Editorials

Big Cells, Little Cells, Stem Cells

Agents of Cardiac Plasticity

Eduardo Marbán

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 536–544


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,1–3 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 . . . [Full Text of this Article]


Related Article:

Adolescent Feline Heart Contains a Population of Small, Proliferative Ventricular Myocytes With Immature Physiological Properties
Xiongwen Chen, Rachel M. Wilson, Hajime Kubo, Remus M. Berretta, David M. Harris, Xiaoying Zhang, Naser Jaleel, Scott M. MacDonnell, Claudia Bearzi, Jochen Tillmanns, Irina Trofimova, Toru Hosoda, Federico Mosna, Leanne Cribbs, Annarosa Leri, Jan Kajstura, Piero Anversa, and Steven R. Houser
Circ. Res. 2007 100: 536-544. [Abstract] [Full Text] [PDF]