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De novo cardiomyocytes from within the activated adult heart after injury

Nicola Smart, Sveva Bollini, Karina N. Dubé, Joaquim M. Vieira, Bin Zhou, Sean Davidson, Derek Yellon, Johannes Riegler, Anthony N. Price, Mark F. Lythgoe, William T. Pu and Paul R. Riley ()
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Nicola Smart: Molecular Medicine Unit, UCL Institute of Child Health, London WC1N 1EH, UK
Sveva Bollini: Molecular Medicine Unit, UCL Institute of Child Health, London WC1N 1EH, UK
Karina N. Dubé: Molecular Medicine Unit, UCL Institute of Child Health, London WC1N 1EH, UK
Joaquim M. Vieira: Molecular Medicine Unit, UCL Institute of Child Health, London WC1N 1EH, UK
Bin Zhou: Children’s Hospital Boston, 300 Longwood Avenue, Boston, Massachusetts 02115, USA
Sean Davidson: The Hatter Cardiovascular Institute, University College London, London WC1E 6HX, USA
Derek Yellon: The Hatter Cardiovascular Institute, University College London, London WC1E 6HX, USA
Johannes Riegler: Centre for Advanced Biomedical Imaging (CABI), University College London, London WC1E 6DD, UK
Anthony N. Price: MRC Clinical Sciences Centre, Faculty of Medicine, Imperial College London, London W12 0NN, UK
Mark F. Lythgoe: Centre for Advanced Biomedical Imaging (CABI), University College London, London WC1E 6DD, UK
William T. Pu: Children’s Hospital Boston, 300 Longwood Avenue, Boston, Massachusetts 02115, USA
Paul R. Riley: Molecular Medicine Unit, UCL Institute of Child Health, London WC1N 1EH, UK

Nature, 2011, vol. 474, issue 7353, 640-644

Abstract: Repairs of the heart The prospect of cell-based therapy in cardiovascular regenerative medicine comes a step closer with the demonstration that a peptide can stimulate a progenitor cell population in the adult heart to act as a source of new cardiomyocytes. The stem or progenitor cells, thought to be derived from the epicardium, are activated by the small actin monomer binding protein thymosin β4, which has previously been shown to restore vascular potential to adult epicardium-derived progenitor cells after injury. The discovery of a resident source of myocardial progenitors will stimulate a search for small molecules and other factors that promote optimal progenitor activation and replacement of destroyed myocardium.

Date: 2011
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DOI: 10.1038/nature10188

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