Abstract
Experimental gene-therapeutic approaches for the prevention of restenosis after balloon angioplasty are the major source of our insight into pathways operative in the process of vascular renarrowing. We now understand that thrombosis and inflammation are the key mechanisms triggering vascular “healing” in response to injury and know a multitude of potential gene-therapeutic strategies to interfere with appositional thrombus formation, proliferation and migration of vascular smooth muscle cells, lesional recruitment of inflammatory cells or excess deposition of extracellular matrix. Thus far, the major limitation for clinical anti-restenotic gene therapy are concerns about the safety and efficacy of vector systems in use for the local overexpression of transgenes, which in turn is one of the most attractive advantages of gene therapy compared to systemic drug therapy. Here, we review the molecular mechanisms operative in postangioplasty restenosis by highlighting their respective gene therapeutic approaches and the current viral and non-viral vector systems.
Keywords: gene therapy, restenosis, balloon angioplasty, inflammation, smooth muscle cell proliferation, adenovirus
Current Vascular Pharmacology
Title: Gene Therapy Approaches for the Prevention of Restenosis
Volume: 2 Issue: 2
Author(s): Christoph W. Kopp and Rainer de Martin
Affiliation:
Keywords: gene therapy, restenosis, balloon angioplasty, inflammation, smooth muscle cell proliferation, adenovirus
Abstract: Experimental gene-therapeutic approaches for the prevention of restenosis after balloon angioplasty are the major source of our insight into pathways operative in the process of vascular renarrowing. We now understand that thrombosis and inflammation are the key mechanisms triggering vascular “healing” in response to injury and know a multitude of potential gene-therapeutic strategies to interfere with appositional thrombus formation, proliferation and migration of vascular smooth muscle cells, lesional recruitment of inflammatory cells or excess deposition of extracellular matrix. Thus far, the major limitation for clinical anti-restenotic gene therapy are concerns about the safety and efficacy of vector systems in use for the local overexpression of transgenes, which in turn is one of the most attractive advantages of gene therapy compared to systemic drug therapy. Here, we review the molecular mechanisms operative in postangioplasty restenosis by highlighting their respective gene therapeutic approaches and the current viral and non-viral vector systems.
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Cite this article as:
Kopp W. Christoph and Martin de Rainer, Gene Therapy Approaches for the Prevention of Restenosis, Current Vascular Pharmacology 2004; 2 (2) . https://dx.doi.org/10.2174/1570161043476438
DOI https://dx.doi.org/10.2174/1570161043476438 |
Print ISSN 1570-1611 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6212 |
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