ArticleNaunyn-Schmiedeberg's archives of pharmacology2021
Interleukin-38 overexpression prevents bleomycin-induced mouse pulmonary fibrosis.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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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
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- Immunobiological Properties and Clinical Applications of Interleukin-38 for Immune-Mediated Disorders: A Systematic Review Study.International journal of molecular sciences · 2021Pooled it
- Advances in understanding the role of interleukins in pulmonary fibrosis (Review).Experimental and therapeutic medicine · 2025Review
- The protective role of muscone in the development of COPD.Frontiers in immunology · 2025Article
- Interleukin-38 overexpression in keratinocytes limits desquamation but does not affect the global severity of imiquimod-induced skin inflammation in mice.Frontiers in immunology · 2024Article
- The decreased serum levels of interleukin-38 in patients with gout and its clinical significance.Frontiers in immunology · 2024Article
- IL-38 alleviates airway remodeling in chronic asthma via blocking the profibrotic effect of IL-36γ.Clinical and experimental immunology · 2023Article
- Exploratory analysis of interleukin-38 in hospitalized COVID-19 patients.Immunity, inflammation and disease · 2022Article
- Clinical relevance and therapeutic potential of IL-38 in immune and non-immune-related disordersEuropean cytokine network · 2022Review
- Pulmonary Protein Oxidation and Oxidative Stress Modulation byAntioxidants (Basel, Switzerland) · 2022Article
- Neutralization of interleukin-38 exacerbates coxsackievirus B3-induced acute myocarditis in mice.Virology journal · 2021Article
- IL-35 subunit EBI3 alleviates bleomycin-induced pulmonary fibrosis via suppressing DNA enrichment of STAT3.Respiratory research · 2021Article
- The interplay of DAMPs, TLR4, and proinflammatory cytokines in pulmonary fibrosis.Journal of molecular medicine (Berlin, Germany) · 2021Review
- Interleukin-36 Cytokine/Receptor Signaling: A New Target for Tissue Fibrosis.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Pulmonary fibrosis is a kind of pulmonary disorder with chronic inflammation and excessive collagen deposition, and its etiology is not clear. Interleukin (IL)-38 is a new member of IL-1 family cytokines, but its role in pulmonary fibrosis has not been elucidated. In this study, a lentivirus expressing IL-38 was injected into the nasal cavity of mice with bleomycin-induced pulmonary fibrosis. We found that IL-38 overexpression reduced the body weight loss and improved the survival of mice induced by bleomycin. Furthermore, IL-38 expression attenuated the pulmonary inflammation and fibrosis damage induced by bleomycin, decreased the production of pro-inflammatory and pro-fibrotic cytokines such as IL-1β, IL-6, IL-17A, monocyte chemoattractant protein-1, and tumor necrosis factor-α, but increased the release of anti-inflammatory cytokine IL-1 receptor antagonist (IL-1Ra) in the lungs of bleomycin-challenged mice. Our data suggest that IL-38 may inhibit bleomycin-induced pulmonary inflammation and fibrosis through its anti-inflammatory effect and regulation of IL-1β/IL-1Ra balance, and IL-38 may be a new strategy for the treatment of pulmonary fibrosis.
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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.