ArticleInternational journal of cell biology2021
IL-17 Is a Key Regulator of Mucin-Galectin-3 Interactions in Asthma.
Article in International journal of cell biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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
7 citing papers in PubMed, 11 citations in OpenAlex.
- Macrophage surface protein Mac-2 mediates inflammatory and stromal stress pathways in doxorubicin-induced cardiac injury.Cardio-oncology (London, England) · 2026Article
- Ferulic Acid Attenuated Interleukin-17A-Induced Lung Inflammation by Modulating Interleukin-17 Signaling and Tissue Remodeling in a Mouse Model.ACS pharmacology & translational science · 2025Article
- Immune activation and mucin dysregulation in pediatric refractoryFrontiers in cellular and infection microbiology · 2025Article
- The Role of Galectins in Asthma Pathophysiology: A Comprehensive Review.Current issues in molecular biology · 2024Review
- Unleashing the Power of IL-17: A Promising Frontier in Chronic Obstructive Pulmonary Disease (COPD) Treatment.Cureus · 2023Review
- Chemokine-mucinome interplay in shaping the heterogeneous tumor microenvironment of pancreatic cancer.Seminars in cancer biology · 2022Review
- Role of Th17 Cytokines in Airway Remodeling in Asthma and Therapy Perspectives.Frontiers in allergy · 2022Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Mucus hypersecretion and chronic airway inflammation are standard characteristics of several airway diseases, such as chronic obstructive pulmonary disease and asthma. Increased mucus secretion from increased mucin gene expression in the airway epithelium is associated with poor prognosis and mortality. We previously showed that the absence of tissue inhibitor of metalloproteinase 1 (TIMP-1) enhances lung inflammation, airway hyperreactivity, and lung remodeling in asthma in an ovalbumin (OVA) asthma model of TIMP-1 knockout (TIMPKO) mice as compared to wild-type (WT) controls and mediated by increased galectin-3 (Gal-3) levels. Additionally, we have shown that in the lung epithelial cell line A549, Gal-3 inhibition increases interleukin-17 (IL-17) levels, leading to increased mucin expression in the airway epithelium. Therefore, in the current study, we further examined the relationship between Gal-3 and the production of IL-17-axis cytokines and critical members of the mucin family in the murine TIMPKO asthma model and the lung epithelium cell line A549. While Gal-3 may regulate a Th
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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 OpenQuestion graph.