ArticleCell death & disease2017
MicroRNA-34/449 targets IGFBP-3 and attenuates airway remodeling by suppressing Nur77-mediated autophagy.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
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Who cites it
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.
- Transcriptomic analysis delineates potential signature genes and miRNAs associated with the pathogenesis of asthma.Scientific reports · 2020Pooled it
- Article
- The Emerging Role of Ly6G⁺Nur77⁺ Lung Macrophages in Type-2 Allergic Inflammation: A Comprehensive Review on Asthma Pathogenesis.Current allergy and asthma reports · 2026Review
- Participation of miRNA-23a-3p in Pulmonary Tuberculosis Through Macrophages via the JAK-STAT Pathway.International journal of chronic obstructive pulmonary disease · 2026Article
- Roles of microRNAs in acute lung injury and acute respiratory distress syndrome: mechanisms and clinical potential.Frontiers in immunology · 2025Review
- Treatment of chronic obstructive pulmonary disease by traditional Chinese medicine Morin monomer regulated by autophagy.Journal of thoracic disease · 2024Article
- Discovering genes and microRNAs involved in human lung development unveils IGFBP3/miR-34a dynamics and their relevance for alveolar differentiation.Stem cell research & therapy · 2024Article
- Bronchial thermoplasty decreases airway remodeling by inhibiting autophagy via the AMPK/mTOR signaling pathway.Acta biochimica et biophysica Sinica · 2024Article
- The role of IGFBP-3 in tumor development and progression: enlightenment for diagnosis and treatment.Medical oncology (Northwood, London, England) · 2024Review
- Nur77 Mediates Anaphylaxis by Regulating miR-21a.Current issues in molecular biology · 2024Article
- Insulin-like growth factor-binding protein-3 is induced by tamoxifen and fulvestrant and modulates fulvestrant response in breast cancer cells.Frontiers in oncology · 2024Article
- Signaling Pathways of the Insulin-like Growth Factor Binding Proteins.Endocrine reviews · 2023Article
- miR-34b/c-5p/CXCL10 Axis Induced by RSV Infection Mediates a Mechanism of Airway Hyperresponsive Diseases.Biology · 2023Article
- New insights into autophagy in inflammatory subtypes of asthma.Frontiers in immunology · 2023Review
- Gene network analysis for identification of microRNA biomarkers for asthma.Respiratory research · 2022Article
- Article
- IGFBP-3 functions as a molecular switch that mediates mitochondrial and metabolic homeostasis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- The Role of Noncoding RNA in Airway Allergic Diseases through Regulation of T Cell Subsets.Mediators of inflammation · 2022Review
- Upregulated IGFBP3 with Aging Is Involved in Modulating Apoptosis, Oxidative Stress, and Fibrosis: A Target of Age-Related Erectile Dysfunction.Oxidative medicine and cellular longevity · 2022Article
- Potential role for EZH2 in promotion of asthma through suppression of miR-34b transcription by inhibition of FOXO3.Laboratory investigation; a journal of technical methods and pathology · 2021Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy plays critical roles in airway inflammation and fibrosis-mediated airway remodeling and many factors including proinflammatory cytokines and inflammation related pathways are involved in the process. The aim of the present study was to examine the role of epithelial microRNAs (miRNAs) in autophagy-mediated airway remodeling and to identify the factors involved and the underlying mechanisms. Serum miR-34/449, inflammatory factors, and autophagy and fibrosis-related proteins were determined by real-time PCR, enzyme-linked immunosorbent assay and western blotting in 46 subjects with asthma and 10 controls and in the lung epithelial cell line BEAS-2B induced with IL-13 and treated with miRNA mimics. Luciferase assays were used to verify IGFBP-3 as a target of miR-34/449, and immunohistochemistry, immunofluorescence and co-immunoprecipitation were used in vitro and in vivo study. miR-34/449 were downregulated in patients with asthma in parallel with the upregulation of autophagy-related proteins. Proinflammatory factors and fibrosis-related proteins were significantly higher in asthma patients than in healthy controls. IL-13 induction promoted autophagy and upregulated miR-34/449 in BEAS-2B cells, and these effects were restored by IGFBP-3 silencing. miR-34/449 overexpression suppressed autophagy, decreased fibrosis, activated Akt, downregulated fibrosis-related factors, and downregulated proinflammatory cytokines and nuclear factor κB by targeting IGFBP-3. In vivo experiments showed that miR-34/449 overexpression was associated with Nur77 nuclear translocation and IGFBP-3 downregulation in parallel with decreased airway remodeling by decreased autophagy. miR-34/449 are potential biomarkers and therapeutic targets in asthma. miR-34/449 may contribute to airway inflammation and fibrosis by modulating IGFBP-3 mediated autophagy activation.
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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.