ArticleCirculation2010
Targeted deletions of cyclooxygenase-2 and atherogenesis in mice.
Article in Circulation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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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.
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Who cites it
33 citing papers in PubMed, 63 citations in OpenAlex.
- The regulation of COX-2, ABCA1, and ABCG1 by the lncRNA PACERR links the inflammatory response and cholesterol homeostasis.Cell reports · 2026Article
- What we know about prostaglandin pathway dysfunction in chronic enteropathies: From endoscopy to molecular diagnosis.Journal of translational internal medicine · 2026Article
- Plaque-Targeted Delivery of Fluoride-Free MXene Nanozyme for Alleviating Atherosclerosis via Sonocatalytic Therapy.Advanced materials (Deerfield Beach, Fla.) · 2025Article
- Atherosclerosis: from lipid-lowering and anti-inflammatory therapies to targeting arterial retention of ApoB-containing lipoproteins.Frontiers in immunology · 2025Review
- Prostanoids in Cardiac and Vascular Remodeling.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- Current Medical Therapy and Revascularization in Peripheral Artery Disease of the Lower Limbs: Impacts on Subclinical Chronic Inflammation.International journal of molecular sciences · 2023Review
- Neural circuits mediating circulating interleukin-1β-evoked fever in the absence of prostaglandin E2 production.Brain, behavior, and immunity · 2022Article
- New horizons in the roles and associations of COX-2 and novel natural inhibitors in cardiovascular diseases.Molecular medicine (Cambridge, Mass.) · 2021Review
- Celecoxib-Loaded Electrospun Fibrous Antiadhesion Membranes Reduce COX-2/PGENeural plasticity · 2021Article
- Regulatory T cells suppress the expression of COX-2 in vulnerable plaque.Heart and vessels · 2020Article
- Subacute treatment of carprofen facilitate splenocardiac resolution deficit in cardiac injury.Journal of leukocyte biology · 2018Article
- Urinary 11-dehydro-thromboxane B2 levels are associated with vascular inflammation and prognosis in atherosclerotic cardiovascular disease.Prostaglandins & other lipid mediators · 2018Article
- Mesenchymal stem cells decrease lung inflammation during sepsis, acting through inhibition of the MAPK pathway.Stem cell research & therapy · 2017Article
- Cytochrome P450 monooxygenase lipid metabolites are significant second messengers in the resolution of choroidal neovascularization.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- The expansive role of oxylipins on platelet biology.Journal of molecular medicine (Berlin, Germany) · 2017Review
- Activation of E-prostanoid 3 receptor in macrophages facilitates cardiac healing after myocardial infarction.Nature communications · 2017Article
- Microsomal Prostaglandin E Synthase-1 Expression by Aortic Smooth Muscle Cells Attenuates the Differentiated Phenotype.Journal of cardiovascular pharmacology · 2016Article
- An Update of Microsomal Prostaglandin E Synthase-1 and PGE2 Receptors in Cardiovascular Health and Diseases.Oxidative medicine and cellular longevity · 2016Review
- Anti-inflammatory therapies for atherosclerosis.Nature reviews. Cardiology · 2015Review
- Clocks and cardiovascular function.Methods in enzymology · 2015Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAlthough the dominant product of vascular Cyclooxygenase-2 (COX-2), prostacyclin (PGI(2)), restrains atherogenesis, inhibition and deletion of COX-2 have yielded conflicting results in mouse models of atherosclerosis. Floxed mice were used to parse distinct cellular contributions of COX-2 in macrophages and T cells (TCs) to atherogenesis. METHODS AND
resultsDeletion of macrophage-COX-2 (Mac-COX-2KOs) was attained with LysMCre mice and completely suppressed lipopolysaccharide-stimulated macrophage prostaglandin (PG) formation and lipopolysaccharide-evoked systemic PG biosynthesis by approximately 30%. Lipopolysaccharide-stimulated COX-2 expression was suppressed in polymorphonuclear leukocytes isolated from MacKOs, but PG formation was not even detected in polymorphonuclear leukocyte supernatants from control mice. Atherogenesis was attenuated when MacKOs were crossed into hyperlipidemic low-density lipoprotein receptor knockouts. Deletion of Mac-COX-2 appeared to remove a restraint on COX-2 expression in lesional nonleukocyte (CD45- and CD11b-negative) vascular cells that express vascular cell adhesion molecule and variably alpha-smooth muscle actin and vimentin, portending a shift in PG profile and consequent atheroprotection. Basal expression of COX-2 was minimal in TCs, but use of CD4Cre to generate TC knockouts depressed its modest upregulation by anti-CD3epsilon. However, biosynthesis of PGs, TC composition in lymphatic organs, and atherogenesis in low-density lipoprotein receptor knockouts were unaltered in TC knockouts.
conclusionsMacrophage-COX-2, primarily a source of thromboxane A(2) and prostaglandin (PG)E(2), promotes atherogenesis and exerts a restraint on enzyme expression by lesional cells suggestive of vascular smooth muscle cells, a prominent source of atheroprotective prostacyclin. TC COX-2 does not detectably influence TC development or function or atherogenesis in mice.
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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.