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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2009;29:10.)
© 2009 American Heart Association, Inc.

Editorials

Vascular Remodeling in Diabetes

Don’t Leave Without Your STAT5

Anna Zampetaki; Qingbo Xu

From the Cardiovascular Division, King’s College London BHF Centre, London, UK.

Correspondence to Professor Qingbo Xu, Cardiovascular Division, King’s College London, 125 Cold Harbour Lane, London SE5 9NU, UK. E-mail qingbo.xu@kcl.ac.uk

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

Diabetes mellitus is associated with increased risk of cardiovascular disease. A widespread endothelial dysfunction, altered production of vasoactive substances and superoxide and modification of the basement membranes, is believed to play a decisive role in the vascular complications observed in diabetes.¹ More importantly perhaps, in diabetic patients collateral vessel development after vascular occlusion is impaired. It seems that in these patients, arteriogenesis, the growing of preexisting arteriolar connections into collateral to restore the blood supply to the ischemic area, is severely affected.^2,3 This process of active vascular remodeling involves the recruitment of circulating monocytes-macrophage subsets that have a strong angiogenic response. Although these circulating angiogenic cells (CAC) do not adopt a typical endothelial phenotype in vitro, they are capable of enhancing neovascularization in a paracrine manner in vivo and are critical regulators of wound healing and tissue regeneration.⁴ Extensive studies have shown that the numbers of circulating angiogenic cells are significantly lower in type II diabetes, and their angiogenic potential is also dramatically diminished. These cells display defective adhesion to the endothelium, reduced proliferation rate, and impaired ability to create new vascular structures.^5–7 Thus, to pursue any therapeutic application it is necessary to identify the signaling pathways and treatments that promote the proliferation and improve the functional capacity of circulating angiogenic cells in diabetes.

See accompanying article on page 114

In this issue of Atherosclerosis, Thrombosis, and Vascular Biology, Dentelli et al⁸ delineate the molecular mechanisms involved in interleukin (IL) 3–induced angiogenic cell expansion. Previous studies by the same . . . [Full Text of this Article]

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Formation of STAT5/PPAR Transcriptional Complex Modulates Angiogenic Cell Bioavailability in Diabetes

Patrizia Dentelli, Antonella Trombetta, Gabriele Togliatto, Annarita Zeoli, Arturo Rosso, Barbara Uberti, Francesca Orso, Daniela Taverna, Luigi Pegoraro, and Maria Felice Brizzi
Arterioscler Thromb Vasc Biol 2009 29: 114-120. [Abstract] [Full Text] [PDF]