2007/11/01 by Colin Funk, Garret A. FitzGerald · 2 citations
Medicine · Biochemistry, Genetics and Molecular Biology · #Inflammatory mediators and NSAID effects #Eicosanoids and Hypertension Pharmacology #Antiplatelet Therapy and Cardiovascular Diseases
paper · doi:10.1097/fjc.0b013e318157f72d
openalex publication_date 2007/11/01 · openalex created_date 2025/10/10 · openalex updated_date 2026/08/04
Placebo-controlled trials of nonsteroidal antiinflammatory drugs (NSAIDs) selective for COX-2 have revealed an enhanced risk for cardiovascular events. COX-2 inhibitors (coxibs) selectively reduce vascular prostacyclin synthesis without disrupting COX-1-derived thromboxane synthesis in platelets. Removal of prostacyclin's capacity to restrain all known endogenous compounds contributing to platelet activation and vasoconstriction is a well-recognized mechanism for coxib action in the cardiovascular system which can pre-dispose to thrombosis, hypertension and atherosclerosis. Novel mouse models of selective COX-2 inhibition and disruption of microsomal prostaglandin E synthase-1 have been exploited to reveal the relative importance of prostacyclin and prostaglandin E2 in cardiovascular homeostasis. This review discusses the background to our current understanding of coxibs and provides further information relating to recent mechanistic insights into how COX-2 inhibition promotes cardiovascular risk.