ArticleRespiratory research2025
IL-5 signaling in asthmatic derived fibroblasts exacerbates airway remodeling through ECM dysregulation and apoptosis resistance.
Article in Respiratory research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Anti-type 2 monoclonal antibody therapy for eosinophilic COPD beyond triple therapy: a systematic review and meta-analysis with strict eosinophil inclusion criteria.Frontiers in medicine · 2026Pooled it
- Beyond Eosinophil Depletion: IL-5 as a Context-Dependent Regulator of Airway Immune Networks.International journal of molecular sciences · 2026Review
- Canonical and emerging regulatory mechanisms of tissue remodeling: shared principles across organs and therapeutic opportunities.Frontiers in immunology · 2026Review
- The Role of BMAL1 in Regulating Circadian Rhythms During Airway Remodeling in Asthma.Journal of immunology research · 2026Review
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
backgroundAirway remodelling, a critical feature of severe asthma, involves fibroblast-driven extracellular matrix (ECM) dysregulation. While IL-5 is pivotal in eosinophilic inflammation, its direct role in fibroblast-mediated fibrosis remains undefined.
methodsPrimary lung fibroblasts from asthmatic and healthy donors were stimulated with 0.5 ng/ml of IL-5 for several time points. ECM components, Matrix metalloproteinases (MMPs), Tissue inhibitor of metalloproteinases (TIMPs), and cytokines were analysed via quantitative real time-PCR (qRT-PCR), Western blot, ELISA, and flow cytometry. RNA sequencing and absolute gene set enrichment analysis (absGSEA) identified signaling pathways. Apoptosis was assessed using Annexin V/PI staining.
resultsIL-5 shown to markedly increase the expression of ECM proteins, including collagen I and fibronectin, in asthmatic fibroblasts. It also upregulated MMP-2 and MMP-3 expression, alongside increased levels of TIMP-1 and TIMP-2. Moreover, IL-5 promoted the secretion of IL-6 and TGF-β. RNA-seq analysis identified 472 differentially expressed genes in asthmatic fibroblasts, highlighting activation of the MAPK pathway and suppression of apoptosis through NR4A1 upregulation. IL-5 further reduced fibroblast apoptosis and enhanced IL-5Rα expression, indicating potential autocrine signalling.
conclusionIL-5 directly activates lung fibroblasts to drive airway remodelling in severe asthma through ECM deposition, MMP/TIMP imbalance, and pro-fibrotic cytokine secretion, positioning it as a dual mediator of inflammation and fibrosis with novel therapeutic potential.
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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.