Advanced Search

Journal Navigation

Journal Home

Subscriptions

Archive

Contact Us

Table of Contents

Click here to browse AJSM online!

Sign In to gain access to subscriptions and/or personal tools.
Vascular Medicine
This Article
Right arrow Full Text (PDF)
Right arrow References
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
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 Saved Citations
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Request Reprints
Right arrow Add to My Marked Citations
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Right arrow Citing Articles via Scopus
Google Scholar
Right arrow Articles by Ehsan, A.
Right arrow Articles by Mann, M. J
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ehsan, A.
Right arrow Articles by Mann, M. J
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Antisense and gene therapy to prevent restenosis

Afshin Ehsan

Department of Medicine, Harvard Medical School and Brigham and Women’s Hospital, Boston, MA, USA

Michael J Mann

Department of Medicine, Harvard Medical School and Brigham and Women’s Hospital, Boston, MA, USA

A primary pathologic response to vascular injury is the proliferation and migration of vascular smooth muscle cells and the development of neointimal lesions. An increasing body of knowledge regarding the molecular and genetic basis of neointimal disease has created a unique opportunity for the treatment of this complex disorder. Gene therapy attempts to correct pathobiological processes by either inhibiting or correcting cellular functions at the level of gene expression. These endpoints are achieved by the delivery of either functional genes or oligonucleotides, capable of interfering with a cell's programmed machinery. Since the early 1990s, the evolution of this technology, along with an ever-expanding source of pathobiological information, has led to many novel approaches for the treatment of restenosis in arterial balloon injury as well as vein graft bypass failure. Using a variety of targets, inhibition of proliferation has predominantly been achieved through direct disruption of the cell cycle machinery. In addition, others have demonstrated successful inhibition by interfering with the signals for cellular proliferation or the enhancement of anti-proliferative stimuli. As this exciting therapeutic alternative evolves, improvements in safety, specificity and efficiency will enhance the likelihood of widespread clinical application.

Key Words: antisense • gene therapy

Vascular Medicine, Vol. 5, No. 2, 103-114 (2000)
DOI: 10.1177/1358836X0000500207


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


This article has been cited by other articles:


Home page
Arterioscler. Thromb. Vasc. Bio.Home page
G. J. Wang, X. X. Sui, H. F. Simosa, M. K. Jain, D. C. Altieri, and M. S. Conte
Regulation of Vein Graft Hyperplasia by Survivin, an Inhibitor of Apoptosis Protein
Arterioscler. Thromb. Vasc. Biol., October 1, 2005; 25(10): 2081 - 2087.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
C. R. Yellaturu and G. N. Rao
A Requirement for Calcium-independent Phospholipase A2 in Thrombin-induced Arachidonic Acid Release and Growth in Vascular Smooth Muscle Cells
J. Biol. Chem., October 31, 2003; 278(44): 43831 - 43837.
[Abstract] [Full Text] [PDF]