title: Nitric oxide and nitrite-based therapeutic opportunities in intimal hyperplasia.
abstract: Vascular intimal hyperplasia (IH) limits the long term efficacy of current surgical and percutaneous therapies for atherosclerotic disease. There are extensive changes in gene expression and cell signaling in response to vascular therapies, including changes in nitric oxide (NO) signaling. NO is well recognized for its vasoregulatory properties and has been investigated as a therapeutic treatment for its vasoprotective abilities. The circulating molecules nitrite (NO(2)(-)) and nitrate (NO(3)(-)), once thought to be stable products of NO metabolism, are now recognized as important circulating reservoirs of NO and represent a complementary source of NO in contrast to the classic L-arginine-NO-synthase pathway. Here we review the background of IH, its relationship with the NO and nitrite/nitrate pathways, and current and future therapeutic opportunities for these molecules.
authors.affiliation: Department of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States.
authors.forename: Matthew J
authors.initials: MJ
authors.lastname: Alef
authors.forename: Edith
authors.initials: E
authors.lastname: Tzeng
authors.forename: Brian S
authors.initials: BS
authors.lastname: Zuckerbraun
mesh_terms: D000818:Animals; D006801:Humans; D006965:Hyperplasia; D009566:Nitrates / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism*; D009573:Nitrites / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects; D017539:Tunica Intima / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D014652:Vascular Diseases / Q000188:drug therapy / Q000378:metabolism*; D014968:Xanthine Dehydrogenase / Q000378:metabolism
chemical_list: D009566:Nitrates; D009573:Nitrites; D009569:Nitric Oxide; D014968:Xanthine Dehydrogenase