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Arteriosclerosis, Thrombosis, and Vascular Biology. 2000;20:1873-1881

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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2000;20:1873.)
© 2000 American Heart Association, Inc.

Brief Reviews

Nitric Oxide Synthase in Atherosclerosis and Vascular Injury

Insights From Experimental Gene Therapy

Keith M. Channon; HuSheng Qian; Samuel E. George

From the Department of Cardiovascular Medicine (K.M.C.), University of Oxford, John Radcliffe Hospital, Oxford, England, and the Division of Cardiology (H.Q., S.E.G.), Duke University Medical Center, Durham, NC.

Correspondence to Keith M. Channon, MD, MRCP, Department of Cardiovascular Medicine, University of Oxford, John Radcliffe Hospital, Oxford, UK OX3 9DU. E-mail keith.channon{at}cardiov.ox.ac.uk

Abstract—Gene therapy aims to intervene in a disease process by transfer and expression of specific genes in a target tissue or organ. Cardiovascular gene therapy in humans remains in its infancy, but in the last decade, experimental gene transfer has emerged as a powerful biological tool to investigate the function of specific genes in vascular disease pathobiology. Nitric oxide synthases, the enzymes that produce nitric oxide, have received considerable attention as potential candidates for vascular gene therapy because nitric oxide has pleiotropic antiatherogenic actions in the vessel wall, and abnormalities in nitric oxide biology are apparent very early in the atherogenic process. In this article, we review the use of nitric oxide synthases in experimental vascular gene therapy and assess the utility of these approaches for investigating the role of nitric oxide in atherosclerosis and their potential for human gene therapy.


Key Words: nitric oxide • atherosclerosis • gene transfer • endothelium • adenovirus




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