Cardiovascular Research Advance Access originally published online on January 15, 2009
Cardiovascular Research 2009 81(4):627-628; doi:10.1093/cvr/cvp018
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org
STIM1: a new therapeutic target in occlusive vascular disease?
Vascular Biology and Atherosclerosis Laboratory, Baker IDI Heart and Diabetes Institute, 75 Commercial Road, Melbourne, VIC 3004, Australia
* Corresponding author. Tel: +61 3 8532 1189; fax: +61 3 8532 1100. E-mail address: alex.agrotis@bakeridi.edu.au
This editorial refers to An essential role for stromal interaction molecule 1 in neointima formation following arterial injury by Rui-Wei Guo et al.,8 pp. 660–668, this issue.
| The first 10% of the full text of this article appears below. |
Improvements in interventional cardiology arising from stent development have significantly increased the efficacy of angioplasty as a primary treatment for atherosclerotic artery disease. Nevertheless, this procedure is still prone to failure in some patients due to the occurrence of neointimal hyperplasia that contributes to restenosis, lumen loss, and reduction in blood flow. In addition, late-stent thrombotic complications may also arise in some instances in which anti-proliferative drug-eluting stents are used, due to compromised reendothelialization subsequent to the angioplasty procedure. The development of neointimal hyperplasia is a complex phenomenon, with multiple mechanisms and molecules being involved. Angioplastic denudation of the endothelial barrier overlying the smooth muscle cell
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Cardiovasc Res 2009 81: 660-668.