Plaque Neovascularization and Antiangiogenic Therapy for Atherosclerosis
Brendan Doyle, MD* and
Noel Caplice, MD, PhD ,*
* Division of Cardiovascular Diseases, Molecular Medicine Program, Mayo Clinic, Rochester, Minnesota
Centre for Research in Vascular Biology, Biosciences Institute, University College Cork, Cork, Ireland
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Figure 1 Mechanisms of Vessel Wall Neovascularization in Atherosclerosis
Increased proangiogenic activity, which may be accompanied by reduced endogenous inhibition of angiogenesis, results in vasa vasorum proliferation and intimal neovascularization. FGF = fibroblast growth factors; HGF = hepatocyte growth factor; PDGF = platelet-derived growth factor; SMC = smooth muscle cell; VEGF= vascular endothelial growth factor. Copyrighted and used with permission of Mayo Foundation for Medical Education and Research.
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Figure 2 Role of Vessel Wall Neovascularization in Plaque Growth
Possible roles for microvessels in disease progression include the supply of cellular and soluble lesion components, enhancement of intraplaque gas exchange, and delivery of metabolic substrates to the plaque core. ICAM = intercellular adhesion molecule; LDL = low-density lipoprotein; VCAM = vascular cell adhesion molecule. Copyrighted and used with permission of Mayo Foundation for Medical Education and Research.
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Figure 3 Intraplaque Hemorrhage
Plaque neovessels are of relatively large caliber and poorly invested with smooth muscle cells, a structural weakness that may be further compromised by matrix degrading enzymes released by inflammatory cells. Intraplaque hemorrhage from these vessels may contribute to plaque instability and/or lesion expansion. MMPs = matrix metalloproteinases. Copyrighted and used with permission of Mayo Foundation for Medical Education and Research.
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