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(Circulation Research. 2006;98:157.)
© 2006 American Heart Association, Inc.

Editorials

Inseparably Tied

Functional and Antioxidative Capacity of Endothelial Progenitor Cells

Judith Haendeler, Stefanie Dimmeler

From Molecular Cardiology, Department of Internal Medicine III, University of Frankfurt, Germany.

Correspondence to Stefanie Dimmeler, Molecular Cardiology, Department of Internal Medicine III, University of Frankfurt, Theodor-Stern-Kai 7, Frankfurt, Germany. E-mail Dimmeler@em.uni-frankfurt.de

See related article, pages 254–261

Key Words: oxidative stress • progenitor cells • neovascularization

An extract of the first 250 words of the full text is provided, because this article has no abstract.

New blood vessel formation is required to increase blood supply to the myocardium or other tissues after critical ischemia. Capillary formation after ischemia can be achieved by the sprouting of preexisting vessels, a process named angiogenesis. However, in the last few years it has become evident that bone marrow–derived circulating endothelial progenitor cells (EPCs) can contribute to and amplify neovascularization. EPCs significantly contribute to adult vessel formation by physically incorporating and promoting vessel growth by paracrine mechanisms.¹ Injected EPCs improve neovascularization of ischemic hind limbs and ischemic hearts in animal models (for review see reference ²). Moreover, initial clinical trials demonstrate that the infusion or injection of bone marrow–derived or circulating progenitor cells augment perfusion and increase the ejection fraction in patients with ischemic heart disease (for review see reference ³).

To contribute to tissue repair, EPCs, and stem cells in general, have to be equipped with antioxidative defense systems to survive in necrotic and ischemic tissues. Interestingly, a high resistance to oxidative stress has been considered a characteristic feature of stem cells.^4,5 Protection against oxidative stress by reactive oxygen species is accomplished by a complex defense system composed of several antioxidative enzymes that reduce the damaging effects of reactive oxygen species (for review see reference ⁶). The most vulnerable organelles to oxidative stress are the mitochondria, because of the permanent potential for the production of superoxide anions. Superoxide anions are converted to hydrogen peroxide by superoxide dismutases, whereas hydrogen peroxide is detoxified by the enzymes catalase and glutathione peroxidase. . . . [Full Text of this Article]

Related Article:

Impaired Angiogenesis in Glutathione Peroxidase-1–Deficient Mice Is Associated With Endothelial Progenitor Cell Dysfunction

Gennaro Galasso, Stephan Schiekofer, Kaori Sato, Rei Shibata, Diane E. Handy, Noriyuki Ouchi, Jane A. Leopold, Joseph Loscalzo, and Kenneth Walsh
Circ. Res. 2006 98: 254-261. [Abstract] [Full Text] [PDF]

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