This Article Full Text Full Text (PDF) Alert me when this article is cited 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 HighWire Citing Articles via Google Scholar Google Scholar Articles by Shah, P. K. Search for Related Content PubMed PubMed Citation Articles by Shah, P. K. Related Collections Restenosis Animal models of human disease Smooth muscle proliferation and differentiation Related Article

(Circulation. 2003;107:2175.)
© 2003 American Heart Association, Inc.

Editorial

Inflammation, Neointimal Hyperplasia, and Restenosis

As the Leukocytes Roll, the Arteries Thicken

Prediman K. Shah, MD

From the Division of Cardiology and Atherosclerosis Research Center, Burns and Allen Research Institute, Department of Medicine, Cedars Sinai Medical Center and David Geffen School of Medicine at the University of California, Los Angeles.

Correspondence to P.K. Shah, MD, Director, Division of Cardiology and Atherosclerosis Research Center, Suite 5347, Cedars Sinai Medical Center, 8700 Beverly Blvd, Los Angeles, CA 90048. E-mail shahp@cshs.org

Key Words: Editorials • inflammation • neointima • restenosis • P-selectin

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

Inflammatory response is triggered when tissues are exposed to a variety of insults. This response consists of a cascade of events that includes release of various chemical mediators and recruitment of circulating blood cells (platelets and leukocytes) to the site of injury and their subsequent activation. The inflammatory response attempts to contain the damaging effects of the insult, leading to recovery from its injurious effects. However, when normal checkpoints that limit continuing or ongoing inflammation fail, inflammatory response can become a liability that leads to a diverse group of diseases, including atherosclerosis and thrombosis. A large body of evidence has implicated inflammation in the initiation, progression, and destabilization of atherosclerotic vascular disease, linking many of the known risk factors to atherothrombosis.^1,2 However, the role of inflammation in other vaso-occlusive disorders, such as neointimal thickening after mechanical injury to arteries during angioplasty and/or stenting, is not as well appreciated. Neointimal thickening after mechanical injury predominantly consists of a fibroproliferative reaction initially involving proliferating smooth muscle cells and later dominated by accumulation of extracellular matrix. Neointimal thickening plays a decisive role in restenosis after stenting because stenting essentially precludes constrictive remodeling, whereas postangioplasty restenosis involves elastic recoil and constrictive or negative vessel wall remodeling (vessel shrinkage) in addition to neointimal thickening. An improved understanding of the molecular mechanisms leading to neointimal thickening after mechanical injury would pave the way for development of novel therapeutic approaches for prevention of restenosis, which has remained the Achilles’ heel of endovascular interventions.

See p 2244

Several . . . [Full Text of this Article]

Related Article:

Single Injection of P-Selectin or P-Selectin Glycoprotein Ligand-1 Monoclonal Antibody Blocks Neointima Formation After Arterial Injury in Apolipoprotein E-Deficient Mice

J. William Phillips, Kurt G. Barringhaus, John M. Sanders, Sean E. Hesselbacher, Ann C. Czarnik, David Manka, Dietmar Vestweber, Klaus Ley, and Ian J. Sarembock
Circulation 2003 107: 2244-2249. [Abstract] [Full Text]

This article has been cited by other articles:

				D. W. Anggrahini, N. Emoto, K. Nakayama, B. Widyantoro, S. Adiarto, N. Iwasa, H. Nonaka, Y. Rikitake, Y. Y. Kisanuki, M. Yanagisawa, et al. Vascular endothelial cell-derived endothelin-1 mediates vascular inflammation and neointima formation following blood flow cessation Cardiovasc Res, April 1, 2009; 82(1): 143 - 151. [Abstract] [Full Text] [PDF]

				G. Li, J. M. Sanders, M. H. Bevard, Z. Sun, J. W. Chumley, E. V. Galkina, K. Ley, and I. J. Sarembock CD40 Ligand Promotes Mac-1 Expression, Leukocyte Recruitment, and Neointima Formation after Vascular Injury Am. J. Pathol., April 1, 2008; 172(4): 1141 - 1152. [Abstract] [Full Text] [PDF]

				P. W. Bedard, V. Clerin, N. Sushkova, B. Tchernychev, T. Antrilli, C. Resmini, J. C. Keith Jr., J. K. Hennan, N. Kaila, S. DeBernardo, et al. Characterization of the Novel P-Selectin Inhibitor PSI-697 [2-(4-Chlorobenzyl)-3-hydroxy-7,8,9,10-tetrahydrobenzo[h] Quinoline-4-carboxylic acid] in Vitro and in Rodent Models of Vascular Inflammation and Thrombosis J. Pharmacol. Exp. Ther., February 1, 2008; 324(2): 497 - 506. [Abstract] [Full Text] [PDF]

				J Butany, K Carmichael, S W Leong, and M J Collins Coronary artery stents: identification and evaluation J. Clin. Pathol., August 1, 2005; 58(8): 795 - 804. [Abstract] [Full Text] [PDF]

				P. H Chong and J. W. Cheng Early Experiences and Clinical Implications of Drug-Eluting Stents: Part 1 Ann. Pharmacother., April 1, 2004; 38(4): 661 - 669. [Abstract] [Full Text] [PDF]