Skip Navigation

Cardiovascular Research 2006 71(1):4-5; doi:10.1016/j.cardiores.2006.05.006
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Takahashi, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Takahashi, M.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2006, European Society of Cardiology

The role of endothelin-1 in vascular remodeling in vivo

Masafumi Takahashi*

Division of Cardiovascular Sciences, Department of Organ Regeneration, Shinshu University Graduate School of Medicine, 3-1-1 Asahi, Matsumoto, Nagano 390-8621, Japan

* Tel.: +81 263 37 3194; fax: +81 263 37 2573. Email address: masafumi@sch.md.shinshu-u.ac.jp

Received 2 May 2006; accepted 5 May 2006

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

See article by Dao et al. [4] (pages 61–68) in this issue.

Vascular smooth muscle cells (VSMCs) are a major component of the arterial wall and play a critical role in the development of occlusive vascular lesions. In normal vessels, VSMCs are quiescent, differentiated, and contractile and function to maintain vascular tone and blood pressure. In pathological processes such as the response to vascular injury, VSMCs undergo a phenotypic transition whereby they proliferate, migrate from the medial to the intimal layer, and lead to neointimal formation and subsequent vascular remodeling. These resultant vascular changes contribute to the pathological basis of atherosclerosis and restenosis that occur . . . [Full Text of this Article]


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
J. Pharmacol. Exp. Ther.Home page
K. Kitada, N. Yui, C. Matsumoto, T. Mori, M. Ohkita, and Y. Matsumura
Inhibition of Endothelin ETB Receptor System Aggravates Neointimal Hyperplasia after Balloon Injury of Rat Carotid Artery
J. Pharmacol. Exp. Ther., December 1, 2009; 331(3): 998 - 1004.
[Abstract] [Full Text] [PDF]


Home page
Cardiovasc ResHome page
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]