ArticleJournal of translational medicine2024
LRRC8A drives NADPH oxidase-mediated mitochondrial dysfunction and inflammation in allergic rhinitis.
Article in Journal of translational medicine, 2024. 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.
- LRRC8D Suppresses Prostate Cancer Growth and Enhances Platinum Sensitivity via Modulation of CAV-1/STAT3 Signaling.Membranes · 2026Article
- PBX3 regulates mast cell parthanatos via TOP2A mediated DNA damage in allergic rhinitis.iScience · 2026Article
- LRRC8A Inhibition Overcomes Chemoresistance by Downregulating MRP3 and CYP3A4 in the 3D Spheroid Model of Human Breast Cancer Cells.International journal of molecular sciences · 2026Article
- Phosphoproteomic analysis in a mouse model reveals ERK signaling as a key modulator of inflammatory response in nasal mucosa associated with childhood allergic rhinitis.Frontiers in immunology · 2026Article
- Increased glucose transporter 1 contributes to epithelial barrier dysfunction in allergic rhinitis.The World Allergy Organization journal · 2026Article
- Oxidative stress and reactive oxygen species in otorhinolaryngological diseases: insights from pathophysiology to targeted antioxidant therapies.Redox report : communications in free radical research · 2025Review
- Study of the mechanism of methyltransferase 3 regulation of ferroptosis in allergic rhinitis and promotion of allergic rhinitis in an m6A-dependent mechanism.Journal of inflammation (London, England) · 2025Article
- Treatment with human placental extracts inhibits allergic rhinitis by modulating AMPK/SHP1/SHP2/STING signaling.Molecular medicine reports · 2025Article
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11 authors.
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Abstract
objectivesAllergic rhinitis (AR) is a complex disorder with variable pathogenesis. Increasing evidence suggests that the LRRC8A is involved in maintaining cellular stability, regulating immune cell activation and function, and playing significant roles in inflammation. However, the involvement of LRRC8A in AR inflammation and its underlying mechanisms remain unclear.
methodsLRRC8A expression in AR patients, confirmed by qRT-PCR and Western blotting, was analyzed to investigate its relationship with the clinical characteristics of AR patients. In vitro, IL-13 stimulated HNEpCs to establish a Th2 inflammation model, with subsequent LRRC8A knockout or overexpression. NOX1/NOX4 inhibitor (GKT137831) and chloride channel inhibitor (DCPIB) were utilized to investigate AR development mechanisms during LRRC8A overexpression. An OVA-induced AR model with nasal mucosa LRRC8A knockdown confirmed LRRC8A's regulatory role in AR inflammation.
resultsLRRC8A mRNA and protein levels were significantly elevated in AR patients, positively correlating with NADPH oxidase subunits and Th2 inflammatory markers. In vitro, IL-13 stimulation of HNEpCs resulted in upregulation of LRRC8A and increased expression of NOX1, NOX4, and p22
conclusionLRRC8A drives the upregulation of NOX1, NOX4, and p22
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