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Gene transfer strategies to inhibit neointima formation.

Journal article
Authors Martin F Crook
Levent Akyürek
Published in Trends in Cardiovascular Medicine
Volume 13
Issue 3
Pages 102-6
ISSN 1050-1738
Publication year 2003
Published at Wallenberg Laboratory
Institute of Anatomy and Cell Biology
Pages 102-6
Language en
Keywords Animals, Caenorhabditis elegans, Cell Division, genetics, Drosophila, Gene Therapy, Gene Transfer Techniques, Genetic Vectors, Graft Occlusion, Vascular, prevention & control, Humans, Muscle, Smooth, Vascular, cytology, pathology, Myocytes, Smooth Muscle, pathology, Tunica Intima, cytology, pathology
Subject categories Medical and Health Sciences


Vascular smooth muscle cell (VSMC) proliferation after arterial injury results in neointima formation and plays an important role in the pathogenesis of restenosis after angioplasty, in-stent restenosis, vascular bypass graft occlusion, and allograft vasculopathy. Major progress has been made recently in elucidating the cellular and molecular mechanisms underlying neointima formation. However, no known curative treatment currently exists. In cases in which pharmacologic and surgical interventions have had limited success, gene therapy remains a potential strategy for the treatment of such vascular proliferative diseases. To date, recombinant adenoviral vectors continue to be the most efficient methods of gene transfer into the arterial wall. However, concerns over the safety of using viral vectors in a clinical situation have inspired the considerable progress that has been made in improving both viral and nonviral modes of gene transfer. This review discusses some of the recent insights and outstanding progress in vascular gene therapeutic approaches to inhibit neointima both from a biologic and therapeutic perspective.

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