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Cardiovascular Research Advance Access originally published online on February 4, 2008
Cardiovascular Research 2008 78(1):1-2; doi:10.1093/cvr/cvn026
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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

Divide to survive: myocardial regeneration and functional recovery after cell cycle activation in injured hearts

Alexandre D.T. Costa1,2,*

1 Instituto de Biologia Molecular do Paraná (IBMP), Rua Prof. Algacyr Munhoz Mader 3775, Curitiba, PR, CEP 81350-010, Brazil
2 Instituto Carlos Chagas, Fundação Oswaldo Cruz (FIOCRUZ), Rua Prof. Algacyr Munhoz Mader 3775, Curitiba, PR, CEP 81350-010, Brazil

* Corresponding author. Tel: +55 41 3316 3230/3237; fax: +55 41 3316 3267. E-mail address: adcosta@tecpar.br; adtcosta@gmail.com

This editorial refers to ‘Cardiomyocyte cell cycle activation improves cardiac function after myocardial infarction’ by Hassink et al.,10 pp. 18–25, this issue.

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

Necrotic and apoptotic cell deaths are the two main causes of the heart's loss of cardiac tissue and haemodynamic function after myocardial infarction (MI). The loss of functional cardiac myocytes through necrotic/apoptotic processes during ischaemia in the absence of de novo cell proliferation has been postulated to be a fundamental cause of ventricular remodelling, increased tissue fibrosis, and diminished ventricular pump function.

In the past decade, several approaches have . . . [Full Text of this Article]


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Related articles in Cardiovasc Res:

Cardiomyocyte cell cycle activation improves cardiac function after myocardial infarction
Rutger J. Hassink, Kishore B. Pasumarthi, Hidehiro Nakajima, Michael Rubart, Mark H. Soonpaa, Aart Brutel de la Rivière, Pieter A. Doevendans, and Loren J. Field
Cardiovasc Res 2008 78: 18-25. [Abstract] [FREE Full Text]  

Related Article

Cardiomyocyte cell cycle activation improves cardiac function after myocardial infarction
Rutger J. Hassink, Kishore B. Pasumarthi, Hidehiro Nakajima, Michael Rubart, Mark H. Soonpaa, Aart Brutel de la Rivière, Pieter A. Doevendans, and Loren J. Field
Cardiovasc Res 2008 78: 18-25. [Abstract] [Full Text] [PDF]