Gene therapy for vein graft disease.

Division of Cardiovascular Surgery, Mayo Clinic, 200 First Street SW, Rochester, MN, 55905, USA.
Current Cardiology Reports 02/2001; 3(1):22-8. DOI: 10.1007/s11886-001-0006-0
Source: PubMed

ABSTRACT Applying gene therapeutics to vein graft disease requires foundational knowledge of the underlying pathophysiology. This review details a brief description of vein graft disease, examines published and unpublished data on gene transfer to veins, and reviews the genes, which have significantly altered vascular biology.

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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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