Role of inducible nitric oxide synthase in transplant arteriosclerosis

Paul C. Lee*, Larry L. Shears, Timothy R. Billiar

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

10 Scopus citations


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.

Original languageEnglish
Pages (from-to)1013-1015
Number of pages3
JournalClinical and Experimental Pharmacology and Physiology
Issue number12
StatePublished - 1999
Externally publishedYes


  • Allografts
  • Gene therapy
  • Gene transfer
  • Inducible nitric oxide synthase
  • Intimal hyperplasia
  • Nitric oxide
  • Transplant arteriosclerosis
  • Transplant vasculopathy


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