ArticleScientific reports2013
Cysteinyl leukotrienes regulate endothelial cell inflammatory and proliferative signals through CysLT₂ and CysLT₁ receptors.
Article in Scientific reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.
- Myocardial Infarction andCardiovascular therapeutics · 2021Pooled it
- Autocrine CysLTOncogene · 2026Article
- Intracellular NADJournal of cellular and molecular medicine · 2026Article
- Platelet-mast cell dialogue in innate immune response and inflammation.American journal of physiology. Lung cellular and molecular physiology · 2026Review
- Unraveling cysteinyl leukotrienes and their receptors in inflammation through the brain-gut-lung axis.Virulence · 2025Review
- Roles of Lipoxygenases in Cardiovascular Diseases.Journal of cardiovascular translational research · 2025Review
- Leukotrienes: Bridging the Inflammatory Gap in Asthma and Inflammatory Bowel Diseases (IBD).Comprehensive Physiology · 2025Review
- Article
- Disruption of Swell1/VRAC function impairs initial hemodynamics and activates compensatory leukotriene signaling in zebrafish circulation development.Frontiers in cell and developmental biology · 2025Article
- Spatial metabolomics reveal metabolic alternations in the injured mice kidneys induced by triclocarban treatment.Journal of pharmaceutical analysis · 2024Article
- Eicosanoids Signals in SARS-CoV-2 Infection: A Foe or Friend.Molecular biotechnology · 2024Review
- Altered Expression of CYSLTR1 is Associated With Adverse Clinical Outcome in Triple Negative Breast Tumors: AnEuropean journal of breast health · 2023Article
- Article
- Montelukast and Acute Coronary Syndrome: The Endowed Drug.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Single-cell RNA sequencing of mast cells in eosinophilic esophagitis reveals heterogeneity, local proliferation, and activation that persists in remission.The Journal of allergy and clinical immunology · 2022Article
- A Dual Role for Cysteinyl Leukotriene Receptors in the Pathogenesis of Corneal Infection.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Review
- Eicosanoids in inflammation in the blood and the vessel.Frontiers in pharmacology · 2022Review
- 1,4-dihydroxy quininib modulates the secretome of uveal melanoma tumour explants and a marker of oxidative phosphorylation in a metastatic xenograft model.Frontiers in medicine · 2022Article
- Molecules related to diabetic retinopathy in the vitreous and involved pathways.International journal of ophthalmology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Cysteinyl leukotrienes (cys-LTs), LTC₄, LTD₄, LTE₄ are potent inflammatory lipid mediators that act through two distinct G-protein-coupled receptors, CysLT₁R and CysLT₂R. Although cys-LTs are shown to induce vascular leakage and atherosclerosis, the molecular mechanism by which cys-LTs modulate endothelial function is not known. Here, we show that cys-LTs (LTC₄ and LTD₄) induce robust calcium influx in human umbilical vein endothelial cells (HUVECs) through CysLT₂R, but not CysLT₁R. Further, cys-LT treatment induced endothelial cell (EC) contraction leading to monolayer disruption via CysLT₂R/Rho kinase dependent pathway. Furthermore, stimulation with cys-LTs potentiated TNFα-induced VCAM-1 expression and leukocyte recruitment to ECs through CysLT₂R. In contrast, we found that both LTC₄ and LTD₄ stimulated EC proliferation through CysLT₁R. Taken together, these results suggest that cys-LTs induce endothelial inflammation and proliferation via CysLT₂R/Rho kinase and CysLT₁R/Erk dependent pathways, respectively, which play critical role in the etiology of cardiovascular diseases such as atherosclerosis and myocardial infarction.
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What OpenQuestion holds
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.