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ROLE OF INDUCIBLE NITRIC OXIDE SYNTHASE IN TRANSPLANT ARTERIOSCLEROSIS
Author(s) -
Lee Paul C,
Shears Larry L Shears,
Billiar Timothy R
Publication year - 1999
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1046/j.1440-1681.1999.03183.x
Subject(s) - neointimal hyperplasia , nitric oxide synthase , nitric oxide , arteriosclerosis , mediator , transplantation , medicine , cancer research , immunology , restenosis , stent
SUMMARY 1. Transplant arteriosclerosis is a major obstacle to long‐term allograft survival. Nitric oxide (NO) has been implicated as a mediator in the development of this disease. 2. We and others have shown that inducible nitric oxide synthase (iNOS) is up‐regulated in allografts with transplant arteriosclerosis. Despite the acute cytotoxic effects produced by high levels of NO, a chronic increase in NO availability is protective against neointimal hyperplasia, mainly by suppressing the inflammatory cell recruitment and neointimal smooth muscle cell accumulation. 3. Currently, we have the technology to directly transfer the iNOS gene to allografts. We have demonstrated that this exciting strategy is feasible and therapeutic and may improve the long‐term survival and function of allografts. Future challenges include optimizing the methods and the vectors of gene delivery.