Key result
Direct transfer of the inducible nitric oxide synthase (iNOS) gene to allografts is a feasible therapeutic strategy that may protect against neointimal hyperplasia and improve long-term survival.
Why the study?
Does iNOS gene transfer prevent neointimal hyperplasia and improve survival in allografts?
Does iNOS gene transfer prevent neointimal hyperplasia and improve survival in allografts?
iNOS gene transfer represents a promising therapeutic strategy to prevent transplant arteriosclerosis and improve long-term allograft survival.
iNOS gene transfer merits exploration in transplant vasculopathy; leaves open confirmation of clinical efficacy and safety in prospective trials.
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.
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Lee et al. (1999) conducted a review in Transplant arteriosclerosis. iNOS gene transfer was evaluated. Direct transfer of the inducible nitric oxide synthase (iNOS) gene to allografts is a feasible therapeutic strategy that may protect against neointimal hyperplasia and improve long-term survival.
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