Cyclooxygenase-1, not cyclooxygenase-2, is responsible for physiological production of prostacyclin in the cardiovascular system. - Wikidata - wikimedia - TriplyDB

Cyclooxygenase-1, not cyclooxygenase-2, is responsible for physiological production of prostacyclin in the cardiovascular system.

Cyclooxygenase-1, not cyclooxygenase-2, is responsible for physiological production of prostacyclin in the cardiovascular system.

http://www.wikidata.org/entity/Q36378519

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Effects of Aspirin on Endothelial Function and Hypertension Clinical Pharmacology and Cardiovascular Safety of Naproxen COX-2 protects against atherosclerosis independently of local vascular prostacyclin: identification of COX-2 associated pathways implicate Rgl1 and lymphocyte networks.A systematic review of the effect of paracetamol on blood pressure in hypertensive and non-hypertensive subjects Immunosuppressive/anti-inflammatory cytokines directly and indirectly inhibit endothelial dysfunction--a novel mechanism for maintaining vascular function Prevention of upper gastrointestinal haemorrhage: current controversies and clinical guidance LC-MS/MS confirms that COX-1 drives vascular prostacyclin whilst gene expression pattern reveals non-vascular sites of COX-2 expression Prostaglandin E2 promotes MYCN non-amplified neuroblastoma cell survival via β-catenin stabilization Cyclooxygenases 1 and 2 differentially regulate blood pressure and cerebrovascular responses to acute and chronic intermittent hypoxia: implications for sleep apnea.Role of prostacyclin in pulmonary hypertension.Vasomotor Reaction to Cyclooxygenase-1-Mediated Prostacyclin Synthesis in Carotid Arteries from Two-Kidney-One-Clip Hypertensive Mice.Analgesic Efficacy of Firocoxib, a Selective Inhibitor of Cyclooxygenase 2, in a Mouse Model of Incisional Pain.Novel whole blood assay for phenotyping platelet reactivity in mice identifies ICAM-1 as a mediator of platelet-monocyte interaction Inherited human group IVA cytosolic phospholipase A2 deficiency abolishes platelet, endothelial, and leucocyte eicosanoid generation.Systematic study of constitutive cyclooxygenase-2 expression: Role of NF-κB and NFAT transcriptional pathways Evidence that links loss of cyclooxygenase-2 with increased asymmetric dimethylarginine: novel explanation of cardiovascular side effects associated with anti-inflammatory drugs Differential COX-2 induction by viral and bacterial PAMPs: Consequences for cytokine and interferon responses and implications for anti-viral COX-2 directed therapies.Lymphatic endothelial cells attenuate inflammation via suppression of dendritic cell maturation.Risk of stroke associated with nonsteroidal anti-inflammatory drugs Aging dysregulates D- and E-series resolvins to modulate cardiosplenic and cardiorenal network following myocardial infarction.Aspirin-triggered 15-epi-lipoxin A4 predicts cyclooxygenase-2 in the lungs of LPS-treated mice but not in the circulation: implications for a clinical test.Assessment of nonsteroidal anti-inflammatory drug-induced cardiotoxicity.Comparative evaluation of cardiovascular outcomes in patients with osteoarthritis and rheumatoid arthritis on recommended doses of nonsteroidal anti-inflammatory drugs.Fluid shear stress induces upregulation of COX-2 and PGI2 release in endothelial cells via a pathway involving PECAM-1, PI3K, FAK, and p38.Cardiovascular effects of cyclooxygenase-2 inhibitors: a mechanistic and clinical perspective.The Cardiovascular Pharmacology of Nonsteroidal Anti-Inflammatory Drugs.Increased role of E prostanoid receptor-3 in prostacyclin-evoked contractile activity of spontaneously hypertensive rat mesenteric resistance arteries.Augmented oxidative stress and preserved vasoconstriction induced by hydrogen peroxide in coronary arteries in obesity: role of COX-2.Reply to Ricciotti et al.: Evidence for vascular COX isoforms.COX-2, the dominant source of prostacyclin.Cyclo-oxygenase-1 or -2-mediated metabolism of arachidonic acid in endothelium-dependent contraction of mouse arteries.Vasoconstrictor role of cyclooxygenase-1-mediated prostacyclin synthesis in non-insulin-dependent diabetic mice induced by high-fat diet and streptozotocin.A vasoconstrictor role for cyclooxygenase-1-mediated prostacyclin synthesis in mouse renal arteries.Kidney Transplantation in a Patient Lacking Cytosolic Phospholipase A2 Proves Renal Origins of Urinary PGI-M and TX-M.Cyclooxygenase-2 Selectively Controls Renal Blood Flow Through a Novel PPARβ/δ-Dependent Vasodilator Pathway.Cardiovascular safety of non-steroidal anti-inflammatory drugs revisited.Microarray analysis of gene expression in the cyclooxygenase knockout mice - a connection to autism spectrum disorder.Vascular dysfunction in the stroke-prone spontaneously hypertensive rat is dependent on constrictor prostanoid activity and Y chromosome lineage.Time to reappraise the therapeutic place of celecoxib.

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P2860

Cyclooxygenase-1, not cyclooxygenase-2, is responsible for physiological production of prostacyclin in the cardiovascular system.

http://www.wikidata.org/entity/Q36378519

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Cyclooxygenase-1, not cyclooxy ...... in the cardiovascular system.

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PNAS.1209192109

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Proceedings of the National Academy of Sciences of the United States of America

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Cyclooxygenase-1, not cyclooxy ...... in the cardiovascular system.

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Jane A Mitchell

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Louise S Harrington

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Malak Al-Yamani

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Nicholas S Kirkby

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Oladipupo Adeyemi

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Philip D M Leadbeater

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P2860

Cardiovascular risk with non-steroidal anti-inflammatory drugs: systematic review of population-based controlled observational studies

Expression of a mitogen-responsive gene encoding prostaglandin synthase is regulated by mRNA splicing

Cyclooxygenases 1 and 2

Cyclooxygenases, microsomal prostaglandin E synthase-1, and cardiovascular function

Vascular COX-2 modulates blood pressure and thrombosis in mice.

Thrombosis is reduced by inhibition of COX-1, but unaffected by inhibition of COX-2, in an acute model of platelet activation in the mouse

Selective cyclooxygenase-2 inhibition directly increases human vascular reactivity to norepinephrine during acute inflammation.

Pharmacology of cyclooxygenase-2 inhibition in the kidney.

Biological basis for the cardiovascular consequences of COX-2 inhibition: therapeutic challenges and opportunities.

Double-label expression studies of prostacyclin synthase, thromboxane synthase and COX isoforms in normal aortic endothelium.

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Ginger Lohr Milne

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