Nitrite-generated nitric oxide to protect against intimal hyperplasia formation.
Vascular disease is a leading cause of morbidity and mortality worldwide. Current vascular therapeutic interventions directed at diseased vessels are restricted in long-term efficacy by the development of intimal hyperplasia and the reformation of flow-limiting disease. The vascular injury and inflammation that ensues from the intervention, especially in the setting of an existing atherosclerotic vascular disease, results in further endothelial dysfunction and subsequent smooth muscle cell proliferation and migration. Although the etiology of intimal hyperplasia is multifactorial, impaired nitric oxide (NO) signaling has been implicated. The vasoprotective properties of NO have been intensely studied, and many investigations have focused on harnessing this biological system for therapeutic benefit. Continued studies investigate the role of impaired NO signaling via the classical arginine/NO synthase (NOS)/NO pathway in the setting of intimal hyperplasia. Furthermore, the possible protective effects of nitrate and nitrite-generated NO via non-NOS-mediated pathways to limit vascular injury have been recently appreciated and will likely prove to be an important vasoregulatory and vasoprotective signaling pathway.
University of Pittsburgh, Pittsburgh, PA 15240, USA.
Bilal
B
Ataya
Edith
E
Tzeng
Brian S
BS
Zuckerbraun
D006801:Humans; D006965:Hyperplasia / Q000517:prevention & control; D009569:Nitric Oxide / Q000378:metabolism / Q000502:physiology*; D052250:Nitric Oxide Synthase Type III / Q000502:physiology*; D015398:Signal Transduction; D017539:Tunica Intima / Q000378:metabolism / Q000503:physiopathology*
D009569:Nitric Oxide; D052250:Nitric Oxide Synthase Type III