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Inducible nitric oxide synthase and vascular injury
- Source :
- Cardiovascular Research. 43:650-657
- Publication Year :
- 1999
- Publisher :
- Oxford University Press (OUP), 1999.
-
Abstract
- 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.
- Subjects :
- Vascular smooth muscle
Platelet Aggregation
Endothelium
Physiology
Nitric Oxide Synthase Type II
Biology
Pharmacology
Nitric Oxide
Muscle, Smooth, Vascular
Catheterization
Nitric oxide
chemistry.chemical_compound
Cell Movement
Physiology (medical)
medicine
Animals
Humans
Vascular disease
Arteries
Genetic Therapy
medicine.disease
Vasoprotective
Nitric oxide synthase
Endothelial stem cell
Transplantation
medicine.anatomical_structure
chemistry
Enzyme Induction
Immunology
biology.protein
Heart Transplantation
Endothelium, Vascular
Nitric Oxide Synthase
Cardiology and Cardiovascular Medicine
Cell Division
Subjects
Details
- ISSN :
- 00086363
- Volume :
- 43
- Database :
- OpenAIRE
- Journal :
- Cardiovascular Research
- Accession number :
- edsair.doi.dedup.....b8a4a949a85dc21d3d02f0da153d0d96
- Full Text :
- https://doi.org/10.1016/s0008-6363(99)00130-3