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Cardiovascular Research 2005 65(4):766-767; doi:10.1016/j.cardiores.2005.01.003
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Copyright © 2005, European Society of Cardiology

Role of integrins, including {alpha}8, for neointima formation after vascular injury

Noriko Uesugi and Noriyuki Sakata*

Department of Pathology, School of Medicine, Fukuoka University, Nanakuma 7-45-1 Jonan-ku, Fukuoka city, Fukuoka, 814-0180, Japan

* Corresponding author. Tel.: +81 92 801 1011x3285; fax: +81 92 863 8383. Email address: nysakata@fukuoka-u.ac.jp

Received 28 December 2004; accepted 5 January 2005

The first 10% of the full text of this article appears below.

See article by Z. Zangham and G. Thibault [15] (pages 813–822) in this issue.

Restenosis secondary to intimal hyperplasia is a serious complication of percutaneous transluminal coronary angioplasty, which is caused by smooth muscle cell (SMC) migration and proliferation within the neointima of coronary arteries. The principle function of vascular SMCs (VMSCs) is to maintain vascular tone and resistance. Differentiated SMCs exhibit a contractile phenotype that is characterized by smooth muscle (SM)-specific contractile and cytoskeletal proteins [1]. The other important function of SMCs is related to the response to the repair of the blood vessel wall after vascular injury [1,2]. These responses require modulation of the SM . . . [Full Text of this Article]


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