Inducible nitric oxide synthase and vascular injury

Melina Kibbe*, Timothy Billiar, Edith Tzeng

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

139 Scopus citations


The role nitric oxide (NO) plays in the cardiovascular system is complex and diverse. Even more controversial is the role that the inducible NO synthase enzyme (iNOS) serves in mediating different aspects of cardiovascular pathophysiology. Following arterial injury, NO has been shown to serve many vasoprotective roles, including inhibition of platelet aggregation and adherence to the site of injury, inhibition of leukocyte adherence, inhibition of vascular smooth muscle cell (VSMC) proliferation and migration, and stimulation of endothelial cell (EC) growth. These properties function together to preserve a normal vascular environment following injury. In this review, we discuss what is known about the involvement of iNOS in the vascular injury response. Additionally, we discuss the beneficial role of iNOS gene transfer to the vasculature in preventing the development of neointimal thickening. Lastly, the pathophysiology of transplant vasculopathy is discussed as well as the role of iNOS in this setting.

Original languageEnglish
Pages (from-to)650-657
Number of pages8
JournalCardiovascular Research
Issue number3
StatePublished - 15 Aug 1999
Externally publishedYes


  • Inducible nitric oxide synthase
  • Nitric oxide
  • Vascular injury
  • Vasoprotection


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