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Cardiovascular Research Advance Access originally published online on September 8, 2008
Cardiovascular Research 2008 80(2):161-162; doi:10.1093/cvr/cvn241
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org

Manipulating myocyte cell cycle control for cardiac repair

Thomas A. Gorr1 and Alexander Deten2,*

1 Institute for Veterinary Physiology, University of Zurich, Winterthurerstr. 260, 8057 Zurich, Switzerland
2 Fraunhofer Institute for Cell Therapy and Immunology, Perlickstr. 1, 04103 Leipzig, Germany

* Corresponding author. Tel: +49 341 972 5810; fax: +49 341 972 5809. E-mail address: alexander.deten@izi.fraunhofer.de

This editorial refers to ‘Cardiomyocyte proliferation and protection against post-myocardial infarction heart failure by cyclin D1 and Skp2 ubiquitin ligase’ by Tamamori-Adachi et al.,11 pp. 181–190, this issue.

The first 10% of the full text of this article appears below.

A fundamental tenet in cardiac biology, namely that the heart is a postmitotic organ incapable of regeneration, has recently been challenged. According to the traditional belief, the number of cardiac myocytes we are born with is all we will have for the rest of our lives. If myocytes die (e.g. as the result of infarction), they cannot be renewed. This is why myocardial infarction (MI) and its consequences, such as congestive heart failure, continue to be a major cause of death worldwide despite the considerable therapeutic advances that have been made over the past decades.

In one attempt to evade this dilemma, cell replacement strategies are currently being investigated for their therapeutic potential to restore cardiac function. Indeed, a growing body of evidence from both basic animal studies and . . . [Full Text of this Article]


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Cardiomyocyte proliferation and protection against post-myocardial infarction heart failure by cyclin D1 and Skp2 ubiquitin ligase
Mimi Tamamori-Adachi, Hiromitsu Takagi, Kimio Hashimoto, Kazumichi Goto, Toshinori Hidaka, Uichi Koshimizu, Kazuhiko Yamada, Ikuko Goto, Yasuhiro Maejima, Mitsuaki Isobe, Keiichi I. Nakayama, Norio Inomata, and Shigetaka Kitajima
Cardiovasc Res 2008 80: 181-190. [Abstract] [Full Text] [PDF]