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Cardiovascular Research Advance Access originally published online on April 7, 2009
Cardiovascular Research 2009 82(3):388-389; doi:10.1093/cvr/cvp111
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

When p66ShcA is away, mice EPCs sweetly play

Julie Sainz1 and Masataka Sata2,*

1 INSERM U833, Collège de France, Paris, France
2 Department of Cardiovascular Medicine, Institute of Health Biosciences, The University of Tokushima Graduate School, 3-18-15 Kuramoto-cho, Tokushima 770-8503, Japan

* Corresponding author. Tel: +81 88 633 7850; fax: +81 88 633 7894. E-mail address: sata@clin.med.tokushima-u.ac.jp

This editorial refers to ‘p66ShcA modulates oxidative stress and survival of endothelial progenitor cells in response to high glucose’ by V. Di Stefano et al.,7 pp. 421–427, this issue.

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

Vascular complications represent a major issue in the setting of diabetes. They may ultimately lead to myocardial infarction, stroke, and limb ischaemia in diabetic patients. Under healthy conditions, detrimental effects induced by ischaemia or vascular injuries can be partially counterbalanced by the mobilization of circulating endothelial progenitor cells (EPCs), which participate in compensatory angiogenesis and vascular repair. However, recent reports suggested that the contribution of EPCs to such rescue processes is impaired in diabetic patients.1

Deleterious effects of hyperglycaemia have been linked so far to the activation of four major biochemical pathways: increased polyol pathway flux, increased advanced glycation . . . [Full Text of this Article]


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p66ShcA modulates oxidative stress and survival of endothelial progenitor cells in response to high glucose
Valeria Di Stefano, Chiara Cencioni, Germana Zaccagnini, Alessandra Magenta, Maurizio C. Capogrossi, and Fabio Martelli
Cardiovasc Res 2009 82: 421-429. [Abstract] [Full Text] [PDF]