COX-2 and prostaglandins in atherosclerosis

Arachidonic acid metabolism is involved in acute ischemic syndromes affecting the coronary or cerebrovascular territory, as demonstrated by biochemical measurements of eicosanoid biosynthesis and the results of inhibitor trials in these settings. In particular, the efficacy of low-dose aspirin in re...

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Bibliographic Details
Published in:Lupus 2005-01, Vol.14 (9), p.756-759
Main Author: Cipollone, F
Format: Article
Language:English
Subjects:
Acids
Angioplasty
Arachidonic Acid - metabolism
Asymptomatic
Atherosclerosis
Atherosclerosis - metabolism
Atherosclerosis - pathology
Biosynthesis
Cyclooxygenase 2 - metabolism
Enzymes
Humans
Intramolecular Oxidoreductases - metabolism
Ischemia
Isoenzymes - metabolism
Lipocalins
Lupus
Membrane Proteins - metabolism
Metabolism
Metabolites
Prostaglandin-E Synthases
Prostaglandins - metabolism
Receptors, Prostaglandin E - metabolism
Tumor necrosis factor-TNF
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Summary:Arachidonic acid metabolism is involved in acute ischemic syndromes affecting the coronary or cerebrovascular territory, as demonstrated by biochemical measurements of eicosanoid biosynthesis and the results of inhibitor trials in these settings. In particular, the efficacy of low-dose aspirin in reducing the complications of acute ischemic syndromes has focused attention on the cyclooxygenase (COX) pathway of arachidonic acid metabolism and its products, collectively termed prostanoids. Two cyclooxygenase (COX)-isozymes have been characterized, COX-1 and COX-2, that differ in terms of regulatory mechanisms of expression, tissue distribution, substrate specificity and preferential coupling to upstream and downstream enzymes. While the role of platelet COX-1 in acute ischemic diseases is firmly established, the role of COX-2 in atherothrombosis is still uncertain. Studies from our group suggest that variable expression of upstream and downstream enzymes in the prostanoid biosynthesis may represent important determinants of the functional consequences of COX-2 expression and inhibition in different clinical settings.
ISSN:0961-2033
1477-0962
DOI:10.1191/0961203305lu2215oa