ArticleInflammation2025
Fibroblast Growth Factor 21 Confers Protection Against Asthma Through Inhibition of NLRP3 Inflammasome Activation.
Article in Inflammation, 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.
- The dual role of mTOR in multiple sclerosis pathophysiology: a systematic review.Journal of neurology · 2026Pooled it
- Potential Biomarkers for Disease Stratification and Prognosis Prediction in Pediatric Asthma: LCN2, sST2 and FGF21.The Kaohsiung journal of medical sciences · 2026Article
- HMGB1 blockade attenuates cardiac injury induced by radiotherapy combined with PD-1 inhibitor while maintaining the anti-tumor efficacy.Apoptosis : an international journal on programmed cell death · 2026Article
- FGF21 Exacerbates Obesity-Induced Airway Hyperresponsiveness and FGFR1-Dependent Mast Cell Activation in Mice.Journal of inflammation research · 2026Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibroblast growth factor 21 (FGF21) modulates the inflammatory response in a range of pathological conditions. However, whether FGF21 modulates asthma remains unexplored. This study sought to investigate its function in asthma using an ovalbumin (OVA)-induced mouse model. Levels of FGF21 were observed to be elevated in mice exhibiting asthmatic symptoms. FGF21 knockout (KO) mice exhibited exacerbated asthmatic pathologies, marked by heightened infiltration of inflammatory cells and elevated release of inflammatory cytokine, compared to wild-type (WT) mice with OVA challenge. Adeno-associated virus (AAV)-mediated overexpression of FGF21 significantly reversed asthmatic pathologies in both WT and FGF21 KO mice. Activated NLRP3 inflammasome was observed in WT mice following OVA challenge, and this response was intensified in FGF21 KO mice, manifested by an upregulation of NLRP3, ASC, cleaved Caspase-1, cleaved Gasdermin D (GSDMD), IL-1β, and IL-18. Pharmacological suppression of NLRP3 ameliorated the aggravated asthmatic pathologies observed in FGF21 KO mice after OVA challenge. Overall, the present work underscores the pivotal function of FGF21 in the pathogenesis of asthma and suggests that FGF21 could serve as a potential target for therapeutic interventions.
Indexed as
Identifiers
39730972What Socratic 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 Socratic graph.