ArticleThe Journal of allergy and clinical immunology2022
Retinoic acid promotes fibrinolysis and may regulate polyp formation.
Article in The Journal of allergy and clinical immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Integrated Immune, Epithelial and Lipid Pathways in NSAID-Exacerbated Respiratory Disease.Clinical and translational allergy · 2026Review
- Decreased Production of Tissue Plasminogen Activator in Endothelial Cells From Nasal Polyps.World journal of otorhinolaryngology - head and neck surgery · 2026Article
- Dysregulated glycosaminoglycan biosynthesis and retinoid metabolism in chronic rhinosinusitis with nasal polyps: insights from a comprehensive transcriptomic analysis.Frontiers in immunology · 2026Article
- Clinical and mechanistic advancements in aspirin exacerbated respiratory disease.The Journal of allergy and clinical immunology · 2025Review
- Visual and bibliometric analysis of chronic rhinosinusitis and nasal polyps.The journal of allergy and clinical immunology. Global · 2024Article
- Retinoic acid mitigates the NSC319726-induced spermatogenesis dysfunction through cuproptosis-independent mechanisms.Cell biology and toxicology · 2024Article
- Retinoic Acid Treatment Mitigates PM2.5-Induced Type 2 Inflammation: Insights into Modulation of Innate Immune Responses.International journal of molecular sciences · 2024Article
- Mechanistic and clinical updates in AERD: 2021-2022.The Journal of allergy and clinical immunology · 2023Article
Corrections and comments
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Authors and funding
27 authors at 6 institutions in 3 countries.
Funding
Abstract
backgroundPatients with aspirin-exacerbated respiratory disease (AERD) regularly exhibit severe nasal polyposis. Studies suggest that chronic rhinosinusitis with nasal polyps (CRSwNP) is characterized by excessive fibrin deposition associated with a profound decrease in epithelial tissue plasminogen activator (tPA). Retinoids, including vitamin A and its active metabolite retinoic acid (RA), are necessary for maintaining epithelial function and well-known inducers of tPA in endothelial cells.
objectivesThis study sought to determine whether endogenous retinoids are involved in NP pathophysiology and disease severity in patients with CRSwNP and AERD.
methodsNP tissue was collected from patients with AERD or CRSwNP, and concentrations of retinoids and fibrinolysis markers were measured using ELISA. Normal human bronchial epithelial cells were stimulated alone or in combination with RA and IL-13 for 24 hours.
resultsThis study observed lower retinoid levels in nasal polyps of patients with AERD than those with CRSwNP or healthy controls (P < .01). Levels of the fibrin-breakdown product d-dimer were the lowest in AERD polyps (P < .01), which is consistent with lower tPA expression (P < .01). In vitro, all-trans RA upregulated tPA levels in normal human bronchial epithelial cells by 15-fold and reversed the IL-13-induced attenuation of tPA expression in cultured cells (P < .01).
conclusionsRA, a potent inducer of epithelial tPA in vitro, is reduced in tissue from patients with AERD, a finding that may potentially contribute to decreased levels of tPA and fibrinolysis in AERD. RA can induce tPA in epithelial cells and can reverse IL-13-induced tPA suppression in vitro, suggesting the potential utility of RA in treating patients with CRSwNP and/or AERD.
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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 Socratic graph.