This Article Full Text Full Text (PDF) All Versions of this Article: 120/2/104    most recent CIRCULATIONAHA.109.873794v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Google Scholar Articles by Simons, M. PubMed PubMed Citation Articles by Simons, M. Pubmed/NCBI databases Substance via MeSH Medline Plus Health Information Diabetes Related Collections Angiogenesis Type 2 diabetes Other Vascular biology Related Article

(Circulation. 2009;120:104-105.)
© 2009 American Heart Association, Inc.

Editorial

Diabetic Monocyte and Vascular Endothelial Growth Factor Signaling Impairment

Michael Simons, MD

From the Section of Cardiovascular Medicine, Department of Internal Medicine, Yale University School of Medicine, New Haven, Conn.

Correspondence to Michael Simons, MD, Section of Cardiovascular Medicine, Department of Internal Medicine, Yale University School of Medicine, 333 Cedar St, New Haven, CT 06520-8017. E-mail michael.simons@yale.edu

Key Words: Editorials • angiogenesis • collateral circulation • diabetes mellitus • growth substances • signal transduction

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

Diabetes mellitus has emerged as a major health problem affecting >20 million Americans and 200 million people worldwide. Diabetes complications are often debilitating and affect the function of multiple organs. Although many complications of diabetes mellitus, including uncontrolled capillary proliferation in the retina, have received extensive attention, a poorly understood complication is an impaired arteriogenic response to macrovascular obstruction. This is manifested in patients with peripheral and coronary arterial occlusion as reduced collateral density and impaired wound healing.^1–4

Article see p 150

The seemingly paradoxical decrease in arteriogenic responsiveness and increase in angiogenesis observed in diabetic patients⁵ present a distinct challenge to vascular biologists but also provide a grand opportunity for a deeper understanding of the fundamental biology of these 2 processes and their regulation. Angiogenesis, a process of capillary growth, is a relatively well-understood event. It is most often encountered in tissue injury settings such as wound healing or in ischemic settings after a proximal arterial occlusion or stenosis. Angiogenesis is driven largely by vascular endothelial growth factor (VEGF) released either by ischemic tissues or by inflammatory cells. The result is acceleration of tissue repair in the case of injury and mild amelioration of ischemia in the case of arterial occlusion.⁶

Arteriogenesis, on the other hand, is a much more complex and much less understood process that refers to formation of new arterial vasculature. This new vasculature may form de novo, presumably by arterialization of the capillary bed, a process that involves acquisition of arterial identity and maturation of . . . [Full Text of this Article]

Related Article:

Diabetes Mellitus Activates Signal Transduction Pathways Resulting in Vascular Endothelial Growth Factor Resistance of Human Monocytes

Vadim Tchaikovski, Servé Olieslagers, Frank -D. Böhmer, and Johannes Waltenberger
Circulation 2009 120: 150-159. [Abstract] [Full Text]