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REVIEW |
Evans Department of Medicine and Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts
Correspondence to:
Correspondence to:
Dr Joseph Loscalzo, Whitaker Cardiovascular Institute, 80 East Concord Street W 507, Boston, MA, USA;
jloscalz{at}bu.edu
The endothelium regulates vascular homoeostasis through local elaboration of mediators that modulate vascular tone, platelet adhesion, inflammation, fibrinolysis, and vascular growth. Impaired vascular function contributes to the pathogenesis of atherosclerosis and acute coronary syndromes. There is growing pathophysiological evidence that increased generation of reactive oxygen species and oxidative stress participates in proatherogenic mechanisms of vascular dysfunction and atherothrombosis. In this review, the role of oxidative stress in mechanisms of vascular dysfunction is discussed, and potential antioxidant strategies are reviewed.
Keywords: atherosclerosis; endothelium; nitric oxide; superoxide
Abbreviations: ACE, angiotensin converting enzyme; EDNO, endothelium-derived nitric oxide; eNOS, endothelial nitric oxide synthase; HOPE (study), Heart Outcomes Prevention Evaluation (study); LDL, low density lipoprotein; MAPK, mitogen activated protein kinase; NADH/NAD(P)H, nicotinamide dinucleotide (phosphate); NF-
B, nuclear factor kappa B; ox-LDL, oxidised low density lipoprotein; SOD, superoxide dismutase
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