ArticleScience translational medicine2012
Vascular COX-2 modulates blood pressure and thrombosis in mice.
Article in Science translational medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
110 citing papers in PubMed, 1 synthesis or guideline pooled it, 233 citations in OpenAlex.
- Cardiovascular safety of NSAIDs: Additional insights after PRECISION and point of view.Clinical cardiology · 2017Pooled it
- Degree of Cyclooxygenase-2 Inhibition Modulates Blood Pressure Response.Hypertension (Dallas, Tex. : 1979) · 2026Trial
- Variability in the Analgesic Response to Ibuprofen Is Associated With Cyclooxygenase Activation in Inflammatory Pain.Clinical pharmacology and therapeutics · 2019Trial
- Cyclooxygenases 1 and 2 differentially regulate blood pressure and cerebrovascular responses to acute and chronic intermittent hypoxia: implications for sleep apnea.Journal of the American Heart Association · 2014Trial
- Single-cell transcriptomics reveals cell-type-specific circadian rhythms and their disruption by acute misalignment in mouse aorta.bioRxiv : the preprint server for biology · 2026Article
- Expert consensus on the application of nonsteroidal anti-inflammatory drugs for perioperative analgesia.Journal of anesthesia and translational medicine · 2026Article
- Cyclomulberrin fromRSC advances · 2026Article
- Prostaglandins and the Cardiovascular System.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- The mechanisms and applications of endothelial progenitor cell therapy in the treatment of intracranial aneurysm.Journal of translational medicine · 2025Review
- Beyond pain relief: the thrombosis threat of celecoxib.Therapeutic advances in drug safety · 2025Article
- Prostaglandin ICellular and molecular life sciences : CMLS · 2024Article
- Differential Impact In Vivo of Pf4-ΔCre-Mediated and Gp1ba-ΔCre-Mediated Depletion of Cyclooxygenase-1 in Platelets in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- Article
- Prostanoids in Cardiac and Vascular Remodeling.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- A helping HAND: therapeutic potential of MAGL inhibition against HIV-1-associated neuroinflammation.Frontiers in immunology · 2024Article
- The Emerging Therapeutic Role of Prostaglandin E2 Signaling in Pulmonary Hypertension.Metabolites · 2023Review
- The Safety of Celecoxib as an Acute Treatment for Migraine: A Narrative Review.Pain and therapy · 2023Review
- The Link between Prostanoids and Cardiovascular Diseases.International journal of molecular sciences · 2023Review
- Can Nonsteroidal Anti-Inflammatory Drugs Lead to First-Time Heart Failure in Patients with Diabetes Mellitus Type-2: Is There a Link?Pharmacology · 2023Article
- Article
50 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
Abstract
Prostacyclin (PGI(2)) is a vasodilator and platelet inhibitor, properties consistent with cardioprotection. More than a decade ago, inhibition of cyclooxygenase-2 (COX-2) by the nonsteroidal anti-inflammatory drugs (NSAIDs) rofecoxib and celecoxib was found to reduce the amount of the major metabolite of PGI(2) (PGI-M) in the urine of healthy volunteers. This suggested that NSAIDs might cause adverse cardiovascular events by reducing production of cardioprotective PGI(2). This prediction was based on the assumption that the concentration of PGI-M in urine likely reflected vascular production of PGI(2) and that other cardioprotective mediators, especially nitric oxide (NO), were not able to compensate for the loss of PGI(2). Subsequently, eight placebo-controlled clinical trials showed that NSAIDs that block COX-2 increase adverse cardiovascular events. We connect tissue-specific effects of NSAID action and functional correlates in mice with clinical outcomes in humans by showing that deletion of COX-2 in the mouse vasculature reduces excretion of PGI-M in urine and predisposes the animals to both hypertension and thrombosis. Furthermore, vascular disruption of COX-2 depressed expression of endothelial NO synthase and the consequent release and function of NO. Thus, suppression of PGI(2) formation resulting from deletion of vascular COX-2 is sufficient to explain the cardiovascular hazard from NSAIDs, which is likely to be augmented by secondary mechanisms such as suppression of NO production.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.