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Published on: August 20, 2007
Understanding regulatory pathways of neovascularization in diabetes
Zeshaan N Maan1, Melanie Rodrigues1, Robert C Rennert1
1a Department of Surgery, Stanford University School of Medicine, 257 Campus Drive West, Hagey Building GK-201, Stanford, CA 94305-5148, USA.
Abstract:
Diabetes mellitus and its associated comorbidities represent a significant health burden worldwide. Vascular dysfunction is the major contributory factor in the development of these comorbidities, which include impaired wound healing, cardiovascular disease and proliferative diabetic retinopathy. While the etiology of abnormal neovascularization in diabetes is complex and paradoxical, the dysregulation of the varied processes contributing to the vascular response are due in large part to the effects of hyperglycemia. In this review, we explore the mechanisms by which hyperglycemia disrupts chemokine expression and function, including the critical hypoxia inducible factor-1 axis. We place particular emphasis on the therapeutic potential of strategies addressing these pathways; as such targeted approaches may one day help alleviate the healthcare burden of diabetic sequelae.
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