ArticleActa pharmaceutica Sinica. B2019
Aspirin alleviates endothelial gap junction dysfunction through inhibition of NLRP3 inflammasome activation in LPS-induced vascular injury.
Article in Acta pharmaceutica Sinica. B, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
What it found
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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
57 citing papers in PubMed, 100 citations in OpenAlex.
- Vascular smooth muscle-specific NLRP3 hyperactivation exacerbates arterial intimal hyperplasia in mice.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Targeting Gasdermins for Therapeutic Interventions in Central Nervous System Injury.Neurotoxicity research · 2026Review
- Role of NLRP3 Inflammasome Inhibitors in Endothelial Dysfunction and Vascular Repair.Antioxidants (Basel, Switzerland) · 2026Review
- Vascular Smooth Muscle-Specific NLRP3 Hyperactivation Drives Arterial Intimal Hyperplasia in Mice.Research square · 2026Article
- Aspirin is associated with improved outcomes in sepsis patients with atrial fibrillation: an analysis of the MIMIC-IV and eICU-CRD databases.Frontiers in cardiovascular medicine · 2026Article
- The KEAP1/NRF2 axis controls LPS-induced oxidative stress, inflammasome activation and caspase-1 activity in human endothelial cells.PloS one · 2026Article
- Aspirin use is associated with attenuated risk of severe acute kidney injury in septic patients: a dual-center retrospective analysis from MIMIC-IV and eICU cohorts.Renal failure · 2025Article
- Novel Drug-Testing Platform for Vascular Injury-induced Intimal Hyperplasia Using a Microphysiological System.Advanced healthcare materials · 2025Article
- Metabolic Stress-Induced Choline Kinase α (CHKA) Activation in Endothelial Subpopulation Contributes to Diabetes-Associated Microvascular Dysfunction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Contribution of NLRP3-GSDMD axis to PDGF-BB-induced vascular smooth muscle cell phenotypic transition.American journal of physiology. Cell physiology · 2025Article
- Mitochondrial quality control as a therapeutic target in cardiovascular disease: Mechanistic insights and future directions.Journal of translational internal medicine · 2025Article
- Understanding a Potential Role for the NLRP3 Inflammasome in Placenta-Mediated Pregnancy Complications.American journal of reproductive immunology (New York, N.Y. : 1989) · 2025Review
- Exosomal novel-miRNA-126 mediates vascular endothelial dysfunction by targeting AhR-NLRP3 pathway in nonalcoholic steatohepatitis.Scientific reports · 2025Article
- Microglial NLRP3-gasdermin D activation impairs blood-brain barrier integrity through interleukin-1β-independent neutrophil chemotaxis upon peripheral inflammation in mice.Nature communications · 2025Article
- Coronary Microvascular Dysfunction Is Associated With Augmented Lysosomal Signaling in Hypercholesterolemic Mice.Journal of the American Heart Association · 2024Article
- Exploring COX-Independent Pathways: A Novel Approach for Meloxicam and Other NSAIDs in Cancer and Cardiovascular Disease Treatment.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Coronary Microvascular Dysfunction is Associated with Augmented Lysosomal Signaling in Hypercholesterolemic Mice.bioRxiv : the preprint server for biology · 2024Article
- Immunologic burden links periodontitis to acute coronary syndrome: levels of CD4 + and CD8 + T cells in gingival granulation tissue.Clinical oral investigations · 2024Article
- Inflammation and coronary microvascular disease: relationship, mechanism and treatment.Frontiers in cardiovascular medicine · 2024Review
- Protective Effect and Mechanism of Aspirin Eugenol Ester on Lipopolysaccharide-Induced Intestinal Barrier Injury.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
The loss of endothelial connective integrity and endothelial barrier dysfunction can lead to increased vascular injury, which is related to the activation of endothelial inflammasomes. There are evidences that low concentrations of aspirin can effectively prevent cardiovascular diseases. We hypothesized that low-dose aspirin could ameliorate endothelial injury by inhibiting the activation of NLRP3 inflammasomes and ultimately prevent cardiovascular diseases. Microvascular endothelial cells were stimulated by lipopolysaccharide (2 μg/mL) and administrated by 0.1-2 mmol/L aspirin. The wild type mice were stimulated with LPS (100 μg/kg/day), and 1 h later treated with aspirin (12.5, 62.5, or 125 mg/kg/day) and dexamethasone (0.0182 mg/kg/day) for 7 days. Plasma and heart were harvested for measurement of ELISA and immunofluorescence analyses. We found that aspirin could inhibit NLRP3 inflammasome formation and activation
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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.