Gene Therapy for Vein Graft Disease
Division of Cardiovascular Surgery, Mayo Clinic, 200 First Street SW, Rochester, MN, 55905, USA. Current Cardiology Reports
(Impact Factor: 1.93).
02/2001; 3(1):22-8. DOI: 10.1007/s11886-001-0006-0
In conclusion, much work has focused on the principles of gene transfer, optimization of methods, and candidate genes. Specifically for human saphenous veins, nitric oxide synthase and TIMI have been most fully evaluated. Gene transfer of nitric oxide synthase has been demonstrated to increase nitric oxide production and reduce neointimal hyperplasia in human SVG.
E2F decoy oligodeoxynucleotide has been used in humans undergoing coronary artery bypass grafting, but no significant difference was observed in graft patency, neointimal hyperplasia, or myocardial infarctions.
Available from: Alex Chen
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ABSTRACT: Gene therapy refers to the transfer of specific genes to the host tissue to intervene in a disease process, with resultant alleviation of the symptoms of a particular disease. Cardiovascular gene transfer is not only a powerful technique for studying the function of specific genes in cardiovascular biology and pathobiology, but also a novel and promising strategy for treating cardiovascular diseases. Since the mid-1990s, nitric oxide synthase (NOS), the enzyme that catalyzes the formation of nitric oxide (NO) from L-arginine, has received considerable attention as a potential candidate for cardiovascular gene therapy, because NO exerts critical and diverse functions in the cardiovascular system, and abnormalities in NO biology are apparent in a number of cardiovascular disease processes including cerebral vasospasm, atherosclerosis, postangioplasty restenosis, transplant vasculopathy, hypertension, diabetes mellitus, impotence and delayed wound healing. There are three NOS isoforms, i.e., endothelial (eNOS), neuronal (nNOS) and inducible (iNOS). All three NOS isoforms have been used in cardiovascular gene transfer studies with encouraging results. This review will discuss the rationale of NOS gene therapy in different cardiovascular disease settings and summarize the results of experimental NOS gene therapy from various animal models of cardiovascular disease to date.
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ABSTRACT: The diverse biological effects of nitric oxide (NO) have led to intense research into its roles in vascular physiology and pathophysiology. Using recombinant DNA and gene transfer the effects of endogenous NO production by the family of NO synthase (NOS) enzymes can be elegantly studied in a variety of tissues. In addition, the feasibility of vascular NOS gene therapy has been demonstrated in animal models. However, technical and safety limitations have to be addressed before NOS gene therapy for cardiovascular disease is available for humans. Since NO exerts critical functions in vascular pathology, including atherosclerosis, post-angioplasty restenosis, vein graft atherosclerosis, transplant atherosclerosis and cardiac allograft vasculopathy, this article reviews recent progress in the field with a focus on potential future applications of NOS-modulating therapies.
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