文档介绍：Cardiovascular Diabetology BioMed Central
Original investigation Open Access
Nitric oxide and superoxide dismutase modulate endothelial
progenitor cell function in type 2 diabetes mellitus
Saher Hamed*1,2,4, Benjamin Brenner2,4, Anat Aharon2,4, Deeb Daoud3 and
Ariel Roguin1,4
Address: 1Department of Cardiology, Rambam Health Care Campus, Haifa, Israel, 2Thrombosis & Hemostasis Unit, Rambam Health Care
Campus, Haifa, Israel, 3Department of Endocrinology, Rambam Health Care Campus, Haifa, Israel and 4The Rappaport Faculty of Medicine, Israel
Institute of Technology, Technion, Haifa, Israel
Email: Saher Hamed* - www.******@; Benjamin Brenner - b_******@; Anat Aharon - a_******@;
Deeb Daoud - d_******@; Ariel Roguin - ******@
* Corresponding author
Published: 30 October 2009 Received: 25 July 2009
Accepted: 30 October 2009
Cardiovascular Diabetology 2009, 8:56 doi:-2840-8-56
This article is available from:
© 2009 Hamed et al; licensee BioMed Central Ltd.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (),
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Background: The function of endothelial progenitor cells (EPCs), which are key cells in vascular
repair, is impaired in diabetes mellitus. Nitric oxide (NO) and reactive oxygen species can regulate
EPC functions. EPCs tolerate oxidative stress by upregulating superoxide dismutase (SOD), the