ArticleJournal of inflammation research2025
miR-6089 Alleviates Inflammation and Cell Apoptosis Through Modulating the TLR4 Pathway in Mite-Sensitized Allergic Rhinitis.
Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Molecular profiling and functional analyses of umbilical cord mesenchymal stem cell-derived extracellular vesicles for dry eye diseases.Extracellular vesicles and circulating nucleic acids · 2026Article
- Exploring the Intervention Mechanism of Effective-Component Combination of Bufei Yishen Formula III for Airway Epithelial Barrier Injury: A miRNA-mRNA Regulatory Network Analysis.Journal of inflammation research · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Allergic rhinitis (AR), a chronic inflammatory disease of nasal mucosa, is considered as a classic Th2-mediated disease. We aimed to elucidate the molecular mechanisms and therapeutic potential of microRNAs (miRNAs) in AR. Methods: Nasal mucosa was collected from patients with mite-sensitized AR and non-allergic controls for miRNA and mRNA sequencing. miRNA expression was profiled. GO and KEGG enrichment analyses were conducted. Luciferase reporter assay was implemented to identify potential targets of candidate miRNAs. An AR cell model was established through lipopolysaccharide (LPS) exposure. miR-6089 was overexpressed or downregulated to characterize its roles in the proliferation and apoptosis of human nasal epithelial cells (HNEpC). The relationship between miR-6089 and toll-like receptor 4 (TLR4) was described. PCR and ELISA were applied to quantify the expression levels of miRNAs and mRNAs. Results: A total of 28 miRNAs and 172 mRNAs were identified to be differently expressed in the nasal mucosa of patients with AR compared to controls. The KEGG enrichment analysis showed that TLR signaling pathway, NF-κB signaling pathway, IL-17 signaling pathway and other pathways were significantly enriched in these differentially expressed RNAs. As shown by PCR results, the expression of miR-6089 decreased, and that of TLR4, IL-6, IL-8, and TSLP increased significantly in the nasal mucosa from patients with AR. Dual-luciferase reporter assay showed that miR-6089 directly bound to TLR4. miR-6089 could increase the viability, inhibit apoptosis, and relieve inflammatory response in LPS-induced HNEpC. Furthermore, miR-6089 could regulate the expression of TLR4, IL-6, IL-8, and TSLP in the LPS-induced HNEpC. Conclusion: miR-6089 can alleviate LPS-induced inflammatory response via targeting TLR4 and may serve as a therapeutic target in the treatment of mite-sensitized AR.
Indexed as
Identifiers
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.