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Heart 2001;86:481-482; doi:10.1136/heart.86.5.481
Copyright © 2001 BMJ Publishing Group Ltd & British Cardiovascular Society
Heart 2001;86:481-482 ( November )

Editorial

Can cardiomyocytes divide?

The first 150 words of the full text of this article appear below.

There is no doubt that research in the field of myocardial regeneration has a remarkably exciting future. This is reflected by a recent statement of the special emphasis panel at the National Heart, Lung, and Blood Institute in the USA, which was assigned to identify areas which should be in the focus of cardiovascular research within the next decades.1 It says that we need to acquire " . . .fundamental understanding of stem cell biology, cardiogenic differentiation, and cell cycle control". However, there are certain limitations we face when we want to embark on this field of research:

(1)   the availability of human tissue necessary to study cardiomyocyte division is limited and the heart consists of a heterogenous cell population;
(2)   compared to the contractile protein apparatus there is only a low abundance of most cell cycle regulating factors;
(3)   it may be necessary to convince people that counting cells alone may not give us the right answer about tissue regeneration.

If we wish to make progress in the field of myocardial regeneration in the nearer future, there are a number of issues that need to be addressed:

  • which factors control cell cycle withdrawal in cardiomyocytes?
  • what are their upstream regulators and what are their downstream targets?
  • how do they interact with myogenic differentiation factors?
  • how . . . [Full text of this article]

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This article has been cited by other articles:

  • Buggisch, M., Ateghang, B., Ruhe, C., Strobel, C., Lange, S., Wartenberg, M., Sauer, H. (2007). Stimulation of ES-cell-derived cardiomyogenesis and neonatal cardiac cell proliferation by reactive oxygen species and NADPH oxidase. J. Cell Sci. 120: 885-894 [Abstract] [Full Text]  

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