p66ShcA modulates oxidative stress and survival of endothelial progenitor cells in response to high glucose | Zendy

Valeria Di Stefano | Zendy; Chiara Cencioni | Zendy; Germana Zaccagnini | Zendy; Alessandra Magenta | Zendy; Maurizio C. Capogrossi | Zendy; Fabio Martelli | Zendy

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p66ShcA modulates oxidative stress and survival of endothelial progenitor cells in response to high glucose

Author(s) -

Valeria Di Stefano,

Chiara Cencioni,

Germana Zaccagnini,

Alessandra Magenta,

Maurizio C. Capogrossi,

Fabio Martelli

Publication year - 2009

Publication title -

cardiovascular research

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.774

H-Index - 219

eISSN - 1755-3245

pISSN - 0008-6363

DOI - 10.1093/cvr/cvp082

Subject(s) - oxidative stress , progenitor cell , reactive oxygen species , endothelial progenitor cell , microbiology and biotechnology , apoptosis , mitochondrial ros , stem cell , angiogenesis , oxidative phosphorylation , chemistry , biology , endocrinology , medicine , cancer research , biochemistry

A close relationship exists between hyperglycaemia, oxidative stress, and diabetic complications. In fact, high glucose (HG) determines the overproduction of reactive oxygen species (ROS) by the mitochondria. p66ShcA is a gene that regulates the apoptotic responses to oxidative stress. Indeed, p66ShcA knockout (ko) mice display decreased ROS production and increased resistance to ROS-induced cell death in a variety of pathophysiological settings. Reduced endothelial progenitor cell (EPC) number, differentiation, and function are relevant components of the angiogenesis impairment observed in diabetic patients. We examined the role of p66ShcA in the EPC deficit induced by HG.

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