Choking off Plaque Neovascularity

Abstract

“For every complex problem there is a simple solution—and it’s wrong.” — H.L. Mencken Atherosclerosis is a highly prevalent disease that results from a complex interplay between lipids, endothelial cells, immunoinflammatory cells, cytokines, extracellular matrix, and neovascularization.1 Several lines of evidence suggest that increased adventitial and plaque neovascularity, commonly observed in murine and human atherosclerosis, plays an important role in progression and, possibly, destabilization of atherosclerosis.1–9 Increased plaque neovascularity may contribute to plaque progression by its link to inflammation, as a source of intraplaque hemorrhage and plaque lipid (Figure).1,5,7–9 Schematic illustrates the potential mechanisms of plaque neoangiogenesis and its potential role in atherosclerotic plaque progression. The putative mechanism by which oral DNA Vaccine against Flk-1 (fetal liver kinase or VEGFR2)-expressing cells may inhibits angiogenesis and plaque progression is also shown. The red arrows indicate the potential adverse aspects of such a therapeutic strategy. VEGF indicates vascular endothelial growth factor; VEGFR2, vascular endothelial growth factor receptor 2; IL-8, interleukin-8. See page 1095 The precise mechanisms contributing to increased plaque neovascularity remain to be defined; however, inflammation and one or more angiogenic growth factors have been implicated. One of the pathways for angiogenesis leading to neovascularization involves the family of vascular endothelial growth factor(s) (VEGF) and their receptors (VEGFR). Therefore, VEGF and VEGFR mediated angiogenesis has emerged …