Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation Research
Search: search_blue_button Advanced Search
Circulation Research. 2007;101:323-325
doi: 10.1161/CIRCRESAHA.107.158899
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 Sipido, K. R.
Right arrow Articles by Janssens, S. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sipido, K. R.
Right arrow Articles by Janssens, S. P.
(Circulation Research. 2007;101:323.)
© 2007 American Heart Association, Inc.


Editorials

How Old Is Your Heart?

Karin R. Sipido, Stefan P. Janssens

From the Department of Cardiovascular Medicine, Divisions of Experimental and Clinical Cardiology, University of Leuven and University Hospital, Leuven, Belgium.

Correspondence to Karin R. Sipido, MD, PhD, Laboratory of Experimental Cardiology, KUL, Campus Gasthuisberg O/N 7th floor, Herestraat 49, B-3000 Leuven, Belgium. E-mail Karin.Sipido@med.kuleuven.be



See related articles, pages 387–399


Key Words: stem cells • action potential • Ca2+ handling • cell biology


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 


*    Introduction
 
The traditional concept of the heart as a terminally differentiated postmitotic organ has been largely based on an influential study published in 1925 that reported the paucity or near-absence of cell division and mitosis in the human heart, which was in striking contrast with the regenerative capacity of eg, liver tissue.1 Additional arguments thought to support this concept are the absence of significant tissue regeneration after damage such as myocardial infarction and the response to increased demand of the heart by hypertrophy of cells, rather than by hyperplasia. This concept was, however, challenged a number of years ago. Using improved imaging methods for apoptosis, mitosis, and cellular senescence, Anversa and colleagues provided new quantitative data well beyond what had been reported before; cardiac cells were shown to be capable to reenter the replicative phase, and the incidence of mitotic figures was increased several-fold in the failing heart.2–4 These observations, together with the demonstration of host male cells in gender-mismatched human cardiac transplant recipients,5 formed the basis for developing a new concept of the heart as a dynamic, potentially self-renewing organ. Generation of new myocytes was reported to contribute to remodeling processes.6

Several studies in support of this new paradigm provided evidence for cell division using microscopic confocal imaging. Interestingly, these replicating cells showed a much smaller volume than fully differentiated cardiac myocytes, and it seemed unlikely that the latter would reenter the cell cycle. Subsequently, confocal analysis as well as improved cell isolation and separation techniques identified the existence of . . . [Full Text of this Article]