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Effects of Statins on Transplant Graft Arterial Diseases

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Despite the development of effective immunosuppressive therapy, transplant graft arterial disease (GAD) remains the major limitation to long-term graft survival. Multiple immune and nonimmune risk factors contribute to this vasculopathic disease process; the interplay between host inflammatory cells and donor endothelial cells results in an intimal hyperplastic lesion, whereas alloantigenindependent factors such as prolonged ischemia, surgical manipulation, ischemia-reperfusion injury, and hyperlipidemia may enhance antigen- dependent events, leading to ischemia and graft failure. Several studies suggest that the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, or statins, exert cholesterol-independent immunosuppressive effects beyond their original lipidlowering effects. Clinical studies demonstrate that statins reduce GAD in human cardiac allografts, improving chances for survival, although it remains unclear whether this is secondary to cholesterol-lowering or other mechanisms. Further studies will provide a firm rationale for using statins in organ transplantation.

Keywords: Graft arterial disease; immunosuppressive effects; major histocompatibility complex

Document Type: Research Article

DOI: http://dx.doi.org/10.2174/187152208784587872

Publication date: June 1, 2008

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  • Immunology, Endocrine & Metabolic Agents in Medicinal Chemistry aims to cover all the latest and outstanding developments in the medicinal chemistry and rational drug design for the discovery of new Immunology, Endocrine & Metabolic Agents. Each issue contains a series of timely in-depth reviews written by leaders in the field covering a range of current topics in Immunology, Endocrine & Metabolic medicinal chemistry.

    Immunology, Endocrine & Metabolic Agents in Medicinal Chemistry is an essential journal for every medicinal chemist who wishes to be kept informed and up-to-date with the latest and most important developments in Immunology, Endocrine & Metabolic drug discovery.
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