Abstract
Intimal hyperplasia occurs primarily as a part of the pathogenesis of coronary artery disease or secondary to therapeutic intervention in relieving vascular occlusion. Intimal hyperplasia involving vascular smooth muscle cells is found in atherosclerosis, post-balloon angioplasty restenosis, in-stent restenosis and vein graft disease, predominantly involving the use of saphenous vein conduits in coronary artery bypass grafting procedures. One potentially exciting area is that of gene therapy. Gene and protein expression patterns at the site of vasculoproliferative lesions have been widely studied and several target areas have been identified on the basis of whether the gene has an antiproliferative, proapoptotic, matrix degrading or endothelial protective action. Blood vessels are easily accessible for the delivery of the gene product, and experimental studies using animal models have used catheter-delivered gene products at the site of vascular injury. Currently, the application of antisense technology and adenoviral vector-mediated delivery has shown significant promise, albeit in in vitro or animal model settings. In this review, we discuss the current knowledge in the application of gene therapy in fibroproliferative vasculopathies. We examine some of the cellular mechanisms and intermediaries which could be potential candidates for gene targeting. We also present some of the advances in biomedical technology that might provide useful vehicles for pinpoint delivery of the gene product. Could the future of restenosis treatment be in gene therapy or is it misplaced enthusiasm.
| Original language | English |
|---|---|
| Pages (from-to) | 1185-1198 |
| Number of pages | 14 |
| Journal | Pharmacogenomics |
| Volume | 7 |
| Issue number | 8 |
| DOIs | |
| State | Published - Dec 2006 |
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All Science Journal Classification (ASJC) codes
- Pharmacology
- Genetics(clinical)
Cite this
Gene therapy of fibroproliferative vasculopathies : Current ideas in molecular mechanisms and biomedical technology. / Mitra, Amit K.; Agrawal, Devendra K.
In: Pharmacogenomics, Vol. 7, No. 8, 12.2006, p. 1185-1198.Research output: Contribution to journal › Review article
}
TY - JOUR
T1 - Gene therapy of fibroproliferative vasculopathies
T2 - Current ideas in molecular mechanisms and biomedical technology
AU - Mitra, Amit K.
AU - Agrawal, Devendra K.
PY - 2006/12
Y1 - 2006/12
N2 - Intimal hyperplasia occurs primarily as a part of the pathogenesis of coronary artery disease or secondary to therapeutic intervention in relieving vascular occlusion. Intimal hyperplasia involving vascular smooth muscle cells is found in atherosclerosis, post-balloon angioplasty restenosis, in-stent restenosis and vein graft disease, predominantly involving the use of saphenous vein conduits in coronary artery bypass grafting procedures. One potentially exciting area is that of gene therapy. Gene and protein expression patterns at the site of vasculoproliferative lesions have been widely studied and several target areas have been identified on the basis of whether the gene has an antiproliferative, proapoptotic, matrix degrading or endothelial protective action. Blood vessels are easily accessible for the delivery of the gene product, and experimental studies using animal models have used catheter-delivered gene products at the site of vascular injury. Currently, the application of antisense technology and adenoviral vector-mediated delivery has shown significant promise, albeit in in vitro or animal model settings. In this review, we discuss the current knowledge in the application of gene therapy in fibroproliferative vasculopathies. We examine some of the cellular mechanisms and intermediaries which could be potential candidates for gene targeting. We also present some of the advances in biomedical technology that might provide useful vehicles for pinpoint delivery of the gene product. Could the future of restenosis treatment be in gene therapy or is it misplaced enthusiasm.
AB - Intimal hyperplasia occurs primarily as a part of the pathogenesis of coronary artery disease or secondary to therapeutic intervention in relieving vascular occlusion. Intimal hyperplasia involving vascular smooth muscle cells is found in atherosclerosis, post-balloon angioplasty restenosis, in-stent restenosis and vein graft disease, predominantly involving the use of saphenous vein conduits in coronary artery bypass grafting procedures. One potentially exciting area is that of gene therapy. Gene and protein expression patterns at the site of vasculoproliferative lesions have been widely studied and several target areas have been identified on the basis of whether the gene has an antiproliferative, proapoptotic, matrix degrading or endothelial protective action. Blood vessels are easily accessible for the delivery of the gene product, and experimental studies using animal models have used catheter-delivered gene products at the site of vascular injury. Currently, the application of antisense technology and adenoviral vector-mediated delivery has shown significant promise, albeit in in vitro or animal model settings. In this review, we discuss the current knowledge in the application of gene therapy in fibroproliferative vasculopathies. We examine some of the cellular mechanisms and intermediaries which could be potential candidates for gene targeting. We also present some of the advances in biomedical technology that might provide useful vehicles for pinpoint delivery of the gene product. Could the future of restenosis treatment be in gene therapy or is it misplaced enthusiasm.
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UR - http://www.scopus.com/inward/citedby.url?scp=33845866638&partnerID=8YFLogxK
U2 - 10.2217/14622416.7.8.1185
DO - 10.2217/14622416.7.8.1185
M3 - Review article
VL - 7
SP - 1185
EP - 1198
JO - Pharmacogenomics
JF - Pharmacogenomics
SN - 1462-2416
IS - 8
ER -