Published online before print November 12, 2007, doi: 10.1161/HYPERTENSIONAHA.107.092866
(Hypertension. 2008;51:1.)
© 2008 American Heart Association, Inc.
Brief Reviews |
Maintaining Equilibrium by Selective Targeting of Cyclooxygenase Pathways
Promising Offensives Against Vascular Injury
From the Departments of Pathology and Laboratory Medicine (R.S.D., R.K.U., B.D.L., D.P.H.) and Pharmacology (S.S.G.) and the Center of Vascular Biology (R.S.D., R.K.U., B.D.L., S.S.G., D.P.H.), Weill Cornell Medical College, New York, NY.
Correspondence to David P. Hajjar, Department of Pathology and Laboratory Medicine, Center of Vascular Biology, Room A626, Weill Cornell Medical College, 1300 York Ave, New York, NY 10021. E-mail dphajjar@med.cornell.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
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Introduction |
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Cardiovascular disease is the leading cause of death in most Western countries. Vascular abnormalities associated with cardiovascular disease are attributable to a variety of risk factors, including hypercholesterolemia, hypertension, hyperglycemia, lipotoxicity, obesity, aging, and tobacco smoke.1,2 Importantly, altered ·NO bioavailability is a major underlying mechanism linking each of these risk factors. Indeed, the endothelium is recognized as a pivotal regulator of vascular function by maintaining homeostatic levels of ·NO and prostanoids derived from arachidonic acid (AA) metabolism.3
Eicosanoids, synthesized from unsaturated fatty acids, are biologically active molecules that play a wide range of regulatory roles in the cardiovascular, renal, immune, and gastrointestinal systems.4 Alterations in their biosyntheses can promote hypertension, diabetes, and, in particular, atherosclerosis, an inflammatory disease characterized by the accretion of fat-laden plaques in the arterial wall that can lead to vasoocclusive events. During atherogenesis, eicosanoid production (from the cyclooxygenases [COXs], lipoxygenases [LOXs], and cytochrome P450s pathways) is altered by mechanisms that are not yet well understood. The dichotomous nature of eicosanoids requires that their balance is maintained, and, as such, these pathways are a relevant therapeutic target against cardiovascular disease.5 Thus, it is now appreciated that cardiovascular disease can be triggered by an absolute deficiency of ·NO and/or an imbalance between "beneficial" and "harmful" eicosanoids in the vasculature and that these pathways are mutually interactive. In this review we consider pharmacological therapies possessing the potential for greater safety and efficacy than nonsteroidal antiinflammatory drugs (NSAIDs) in the treatment of chronic vasoinflammatory conditions.
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The Prostaglandin Biosynthesis Quandary |
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Fundamental physiological distinctions are now
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