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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2003;23:1137.)
© 2003 American Heart Association, Inc.

Editorials

Neurogenic Atherosclerosis Mediated by Neuropeptide Y

Hardening of the Evidence

Christopher G. Sobey

From the Department of Pharmacology, The University of Melbourne, Parkville, Australia.

Correspondence to Christopher G. Sobey, Ph. D., Department of Pharmacology, The University of Melbourne, Grattan St, Parkville, Victoria 3010, Australia. E-mail cgsobey@unimelb.edu.au

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

Atherosclerosis is a complex, progressive vascular disease that represents an enormous clinical problem, being the principal cause of myocardial infarction and stroke and responsible for 50% of all mortality in westernized societies.¹ Multiple risk factors for atherosclerosis are known to exist, including hypertension, hyperlipidemia, obesity, and smoking. Treatment of occlusive coronary atherosclerotic plaques is limited to invasive surgical procedures such as angioplasty, stenting, or bypass surgery. Such procedures are effective in acutely restoring blood flow to normal, but restenosis often occurs. For example, in 30% to 40% of patients, restenosis occurs within just 6 months of stenting or angioplasty surgery.² Restenosis is thought to involve generation of vascular smooth muscle growth factors stimulated by various risk factors in the presence of endothelial denudation or dysfunction. However, relatively little attention has been given to the growth-promoting role of nerve-derived factors, even though many vessels that are occluded by atherosclerotic plaques, such as coronary arteries, are richly innervated by sympathetic nerve fibers.

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Endothelial Dysfunction and Neuroendocrine Activation

Endothelial cell dysfunction is widely regarded as a key early phenomenon in the process of atherogenesis.¹ The endothelium normally functions to inhibit vascular cell proliferation by inhibiting platelet aggregation and the release of growth factors from the vascular wall. Endothelial injury therefore commonly results in neointima formation due to proliferating and migrating vascular smooth muscle cells and myofibroblasts. There has been recent interest in whether endothelial dysfunction, and indeed atherosclerosis, can result from activation of the sympathetic nervous system, for example during prolonged stress.³

Potential Importance of Sympathetic Nerves and Neuropeptide Y (NPY) in Atherogenesis

Activation of the . . . [Full Text of this Article]