ArticlePloS one2023
Aspirin modulates production of pro-inflammatory and pro-resolving mediators in endothelial cells.
Article in PloS one, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
- Effects of aspirin on stroke and mortality in tubercular meningitis: a meta-analysis of randomized controlled trials.Frontiers in medicine · 2025Pooled it
- Arachidonic Acid Structure and Synthesis.Reviews of physiology, biochemistry and pharmacology · 2027Review
- Fatty Acid and Oxylipin Metabolism Differentiate Isolated Postcapillary From Combined Pre- and Postcapillary Pulmonary Hypertension.Circulation. Heart failure · 2026Article
- Laser-Generated Ultrashort Pulsed Electron Beams Induce p53-Related Alteration of DNA Repair and Cell Death Pathways in Non-Small Cell Lung Cancer Cells.International journal of molecular sciences · 2026Article
- Aspirin as a neuroprotective scaffold in Alzheimer's disease: inflammation, oxidative stress, and future directions.Molecular biology reports · 2026Review
- Potential Effects of Aspirin on Transcription Factors Related to the Inflammation in Atherosclerosis: A Systematic Review.Health science reports · 2026Review
- Elucidation of a potent pro-resolving mediator of inflammation resolution via human neutrophil-vascular endothelial cell interactions.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- The Potential Role of Endothelial Cells in the Pathophysiology, Diagnosis, and Management of Acute Kawasaki Disease.CJC open · 2026Review
- Mitochondria as Inducers of Neutrophil Extracellular Traps.Inflammation · 2026Review
- Aspirin's effect on macrophages beyond its chemopreventive role in inflammation and cancer.Inflammopharmacology · 2025Review
- P2X7-CaMKII drives 5-LOX nuclear translocation to impair microglial function after subarachnoid hemorrhage.Journal of neuroinflammation · 2025Article
- Antithrombotic therapy in adults with ectatic coronary artery disease: a systematic review and network meta-analysis.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2025Review
- Histopathological Analysis of Lipopolysaccharide-Induced Liver Inflammation and Thrombus Formation in Mice: The Protective Effects of Aspirin.Current issues in molecular biology · 2024Article
- The impact of manganese on vascular endothelium.Toxicological research · 2024Review
- Aspirin pharmacokinetics and pharmacodynamics through gestation.American journal of obstetrics and gynecology · 2024Article
- Aspirin reduces the mortality risk of patients with community-acquired pneumonia: a retrospective propensity-matched analysis of the MIMIC-IV database.Frontiers in pharmacology · 2024Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Endothelial cells synthesize biochemical signals to coordinate a response to insults, resolve inflammation and restore barrier integrity. Vascular cells release a variety of vasoactive bioactive lipid metabolites during the inflammatory response and produce pro-resolving mediators (e.g., Lipoxin A4, LXA4) in cooperation with leukocytes and platelets to bring a halt to inflammation. Aspirin, used in a variety of cardiovascular and pro-thrombotic disorders (e.g., atherosclerosis, angina, preeclampsia), potently inhibits proinflammatory eicosanoid formation. Moreover, aspirin stimulates the synthesis of pro-resolving lipid mediators (SPM), so-called Aspirin-Triggered Lipoxins (ATL). We demonstrate that cytokines stimulated a time- and dose-dependent increase in PGI2 (6-ketoPGF1α) and PGE2 formation that is blocked by aspirin. Eicosanoid production was caused by cytokine-induced expression of cyclooxygenase-2 (COX-2). We also detected increased production of pro-resolving LXA4 in cytokine-stimulated endothelial cells. The R-enantiomer of LXA4, 15-epi-LXA4, was enhanced by aspirin, but only in the presence of cytokine challenge, indicating dependence on COX-2 expression. In contrast to previous reports, we detected arachidonate 5-lipoxygenase (ALOX5) mRNA expression and its cognate protein (5-lipoxygenase, 5-LOX), suggesting that endothelial cells possess the enzymatic machinery necessary to synthesize both pro-inflammatory and pro-resolving lipid mediators independent of added leukocytes or platelets. Finally, we observed that, endothelial cells produced LTB4 in the absence of leukocytes. These results indicate that endothelial cells produce both pro-inflammatory and pro-resolving lipid mediators in the absence of other cell types and aspirin exerts pleiotropic actions influencing both COX and LOX pathways.
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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.