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H. E. von der Leyen, G. H. Gibbons, R. Morishita, et al., “Gene Therapy Inhibiting Neointimal Vascular Lesion: In Vivo Transfer of Endothelial Cell Nitric Oxide Synthase Gene,” Proceedings of the National Academy of Sciences of the United States of America, Vol. 92, No. 4, 1995, pp. 1137-1141. doi:10.1073/pnas.92.4.1137

has been cited by the following article:

• TITLE: Role of Oxidative Stress in Cardiac Allograft Vasculopathy

  AUTHORS: Nandini Nair, Enrique Gongora, Joshua Reynolds

  KEYWORDS: Cardiac Allograft Vasculopathy; Oxidative Stress; Asymmetric Dimethyl Arginine; Cyto Megalo Virus; Transplantation

  JOURNAL NAME: Open Journal of Organ Transplant Surgery, Vol.3 No.2, May 24, 2013

  ABSTRACT: Cardiac Allograft Vasculopathy, an accelerated form of arterial occlusive disease, is the major cause of death in the long-term after heart transplantation. Multiple factors influence the initiation and progression of CAV. These include ischemia-reperfusion, dyslipidemia, insulin resistance, and hypertension due to the use of immunosuppressive agents, the direct effects of immunosuppressive agents on endothelial function, and viruses (CMV). Impaired endothelial function reflects abnormalities in the production or activity of several vasoactive substances. Disruption of the nitric oxide synthase (NOS) pathway leads to changes in vascular reactivity, structure, and interaction with circulating blood components. Since endothelium-derived nitric oxide (NO) suppresses vascular cell proliferation and vascular inflammation, a deficit in vascular NO facilitates development of CAV. The link between oxidative stress and CAV largely exists in the balance between free radical superoxide generation and NO production. This review focuses on identifying the oxidative stress factors affecting CAV.