This Article Full Text Full Text (PDF) Correction (v23,p363) Submit a response Alert me when this article is cited Alert me when eLetters are posted 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 Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Levy, S. E. Articles by Muldowney, J. A.S. Search for Related Content PubMed PubMed Citation Articles by Levy, S. E. Articles by Muldowney, J. A.S., 3rd

(Arteriosclerosis, Thrombosis, and Vascular Biology. 2002;22:1946.)
© 2002 American Heart Association, Inc.

Editorial

Microarray Analysis of Neointima

Flowing Toward a Clear Future

Shawn E. Levy; James A.S. Muldowney, 3rd

From the Department of Molecular Physiology and Biophysics (S.E.L.) and Department of Medicine, Division of Cardiovascular Medicine (J.A.S.M), Vanderbilt University Medical Center, Nashville, Tenn.

Correspondence to Shawn Levy, Department of Molecular Physiology and Biophysics, 702 Light Hall, Vanderbilt University Medical Center, Nashville, TN 37232-0615. E-mail shawn.levy@vanderbilt.edu

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

The blood vessels that comprise the circulatory system are extraordinarily sophisticated and complex. The organization of the cells and extracellular matrix that make up the vessel wall define its structural integrity and regulate vascular physiology and homeostasis through biochemical regulation. The endothelial lining of the normal blood vessel is a continuous, selectively permeable and antithrombotic barrier between the circulating blood and the vessel wall.¹ The endothelium detects shear and humoral signals and in response generates products that regulate blood flow, vessel tone, platelet activation, and thrombosis.^2,3 The endothelium also regulates smooth muscle cell migration and proliferation among its legion of roles.^4–6 Endothelial and vascular injury that are associated with invasive procedures such as angioplasty, vessel and organ transplantation, and coronary and peripheral arterial by-pass surgery, as well as noninvasive phenomenon such as atherosclerosis, disrupt the physical barrier provided by the endothelium, interfering with vascular homeostasis.^7–11 This sets a series of events in motion that lead to a proliferation and migration of smooth muscle cells. Often these proliferative and migratory events extend beyond the normal healing process and result in obstructive arterial lesions. Depending on the exact pathology and mechanism, this process of restenosis or neointimal hyperplasia leads to the failure of bypass grafts, critical narrowings in up to 50% of patients after angioplasty, and proliferative vascular disease in transplanted hearts. While significant advances have been made in the management of restenosis to prevent or reopen these narrowings and innovative treatments continue to be developed, the most effective measures that remain . . . [Full Text of this Article]