ArticleCirculation2011
Microsomal prostaglandin e2 synthase-1 modulates the response to vascular injury.
Article in Circulation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 89 citations in OpenAlex.
- Characterization of a new specific mPGES-1 inhibitor in cardiovascular system.Scientific reports · 2025Article
- Myeloid Cell mPGES-1 Deletion Attenuates Calcium Phosphate-induced Abdominal Aortic Aneurysm in Male Mice.Inflammation · 2025Article
- Exosomes derived from umbilical cord mesenchymal stem cells promote healing of complex perianal fistulas in rats.Stem cell research & therapy · 2024Article
- A highly selective mPGES-1 inhibitor to block abdominal aortic aneurysm progression in the angiotensin mouse model.Scientific reports · 2024Article
- Prostanoids in Cardiac and Vascular Remodeling.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- Novel pharmacological approaches in abdominal aortic aneurysm.Clinical science (London, England : 1979) · 2023Review
- BACH1 deficiency prevents neointima formation and maintains the differentiated phenotype of vascular smooth muscle cells by regulating chromatin accessibility.Nucleic acids research · 2023Article
- Article
- Endothelial Foxp1 Regulates Neointimal Hyperplasia Via Matrix Metalloproteinase-9/Cyclin Dependent Kinase Inhibitor 1B Signal Pathway.Journal of the American Heart Association · 2022Article
- Endothelial Tenascin-X Is Going With the Flow.Circulation research · 2022Article
- Specialized Pro-Resolving Lipid Mediators: New Therapeutic Approaches for Vascular Remodeling.International journal of molecular sciences · 2022Review
- Targeted delivery of mPGES-1 inhibitors to macrophages via the folate receptor-β for inflammatory pain.Bioorganic & medicinal chemistry letters · 2021Article
- Enhanced mPGES-1 Contributes to PD-Related Peritoneal Fibrosis via Activation of the NLRP3 Inflammasome.Frontiers in medicine · 2021Article
- The antiplatelet agent revacept prevents the increase of systemic thromboxane AScientific reports · 2020Article
- International Union of Basic and Clinical Pharmacology. CIX. Differences and Similarities between Human and Rodent Prostaglandin EPharmacological reviews · 2020Article
- The cyclic adenosine monophosphate elevating medicine, forskolin, reduces neointimal formation and atherogenesis in mice.Journal of cellular and molecular medicine · 2020Article
- The Impact of Dietary Supplementation of Whole Foods and Polyphenols on Atherosclerosis.Nutrients · 2020Review
- Pharmacological Characterization of the Microsomal Prostaglandin EFrontiers in pharmacology · 2020Article
- Biological characterization of new inhibitors of microsomal PGE synthase-1 in preclinical models of inflammation and vascular tone.British journal of pharmacology · 2019Article
- Myeloid Cell mPges-1 Deletion Attenuates Mortality Without Affecting Remodeling After Acute Myocardial Infarction in Mice.The Journal of pharmacology and experimental therapeutics · 2019Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
backgroundMicrosomal (m) prostaglandin (PG) E₂ synthase (S)-1 catalyzes the formation of PGE₂ from PGH₂, a cyclooxygenase product that is derived from arachidonic acid. Previous studies in mice suggest that targeting mPGES-1 may be less likely to cause hypertension or thrombosis than cyclooxygenase-2-selective inhibition or deletion in vivo. Indeed, deletion of mPGES-1 retards atherogenesis and angiotensin II-induced aortic aneurysm formation. The role of mPGES-1 in the response to vascular injury is unknown. METHODS AND
resultsMice were subjected to wire injury of the femoral artery. Both neointimal area and vascular stenosis were significantly reduced 4 weeks after injury in mPGES-1 knockout mice compared with wild-type controls (65.6 ± 5.7 versus 37.7 ± 5.1 × 10³ pixel area and 70.5 ± 13.4% versus 47.7 ± 17.4%, respectively; P < 0.01). Induction of tenascin-C, a proproliferative and promigratory extracellular matrix protein, after injury was attenuated in the knockouts. Consistent with in vivo rediversion of PG biosynthesis, mPGES-1-deleted vascular smooth muscle cells generated less PGE₂ but more PGI₂ and expressed reduced tenascin-C compared with wild-type cells. Both suppression of PGE₂ and augmentation of PGI₂ attenuate tenascin-C expression and vascular smooth muscle cell proliferation and migration in vitro.
conclusionsDeletion of mPGES-1 in mice attenuates neointimal hyperplasia after vascular injury, in part by regulating tenascin-C expression. This raises for consideration the therapeutic potential of mPGES-1 inhibitors as adjuvant therapy for percutaneous coronary intervention.
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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.