ArticleNeurosurgery2015
Paradoxical Increase in Mortality and Rupture of Intracranial Aneurysms in Microsomal Prostaglandin E2 Synthase Type 1-Deficient Mice: Attenuation by Aspirin.
Article in Neurosurgery, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- The effect of aspirin on inflammatory response in intracranial aneurysm: a systematic review.Inflammopharmacology · 2025Pooled it
- Aspirin treatment for unruptured intracranial aneurysms: Focusing on its anti-inflammatory role.Heliyon · 2024Review
- Integrated analysis of C3AR1 and CD163 associated with immune infiltration in intracranial aneurysms pathogenesis.Heliyon · 2023Article
- Latest progress in the development of cyclooxygenase-2 pathway inhibitors targeting microsomal prostaglandin EFuture medicinal chemistry · 2022Article
- Endogenous animal models of intracranial aneurysm development: a review.Neurosurgical review · 2021Review
- Metformin inhibits intracranial aneurysm formation and progression by regulating vascular smooth muscle cell phenotype switching via the AMPK/ACC pathway.Journal of neuroinflammation · 2020Article
- Protective Effect of Mesenchymal Stem Cells Against the Development of Intracranial Aneurysm Rupture in Mice.Neurosurgery · 2017Article
- Prostaglandin terminal synthases as novel therapeutic targets.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2017Review
- Differential Sex Response to Aspirin in Decreasing Aneurysm Rupture in Humans and Mice.Hypertension (Dallas, Tex. : 1979) · 2016Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
backgroundInflammation plays an important role in formation and rupture of intracranial aneurysms. Expression of microsomal prostaglandin E2 (PGE2) synthase type 1 (mPGES-1) is increased in the wall of intracranial aneurysms in humans. PGE2, a by-product of mPGES-1, is associated with inflammation and cerebrovascular dysfunction.
objectiveTo test the hypothesis that deletion of mPGES-1 decreases the formation and rupture of intracranial aneurysms in a murine model.
methodsIntracranial aneurysms were induced in wild-type and mPGES-1 knockout (mPGES-1 KO) mice by using a combination of deoxycorticosterone acetate-salt-induced hypertension and intracranial injection of elastase in the basal cistern. Prevalence of aneurysms, subarachnoid hemorrhage, and mortality were assessed. We also tested the effects of administration of aspirin (6 mg/kg/d) by gavage and PGE2 (1 mg/kg/d) by subcutaneous infusion.
resultsSystolic blood pressure and prevalence of aneurysm were similar in wild-type and mPGES-1 KO mice. However, mortality and the prevalence of subarachnoid hemorrhage were markedly increased in mPGES-1 KO mice (P < .05). Bone marrow reconstitution studies suggest that mPGES-1 derived from leukocytes does not appear to increase rupture of intracranial aneurysms. Aspirin, but not PGE2, attenuated the increased mortality in mPGES-1 KO mice (P < .05).
conclusionVascular mPGES-1 plays a protective role in blood vessels and attenuates rupture of cerebral aneurysms. In contrast to effects on abdominal aneurysms, mPGES-1 deficiency is associated with an increase in rupture of cerebral aneurysms and mortality, which are attenuated by low-dose aspirin.
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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.