ArticleFrontiers in immunology2022
Naringenin suppresses BEAS-2B-derived extracellular vesicular cargoes disorder caused by cigarette smoke extract thereby inhibiting M1 macrophage polarization.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- The Effect of Cigarettes and E-Cigarettes on Epithelial-Derived Extracellular Vesicles: A Systematic Review.International journal of molecular sciences · 2026Pooled it
- Reparative "exosome-ark" for mitochondrial transplantation to reprogram macrophages and disrupt pathogenic crosstalk in pulmonary fibrosis.Materials today. Bio · 2026Article
- Pathogen-Specific Regulation of Renin-Angiotensin System Genes in Epithelial Cells: A Comparative Study of SARS-CoV-2 Spike Protein N-Terminal Domain Fragment and Bacterial Lipopolysaccharide.Pathogens (Basel, Switzerland) · 2026Article
- Citrus Peel Flours: From Residues to Bioactive Ingredients for Food Applications.Molecules (Basel, Switzerland) · 2026Article
- Bronchial epithelial-derived exosomal SLC6A14 promotes airway inflammation and mucus hypersecretion via the ZFP36L1/IL-8 axis.Functional & integrative genomics · 2026Article
- MiR-129-5p is associated with chronic obstructive pulmonary disease status and alleviates cigarette smoke extract-induced human bronchial epithelial cell injury.Tobacco induced diseases · 2026Article
- Inhalable extracellular vesicles as cell-free therapeutics for chronic respiratory disease.Frontiers in bioengineering and biotechnology · 2026Review
- Exosomal miR-2110 from PM2.5-Exposed Lung Epithelial Cells Targets SRSF1 to Promote M1 Macrophage Polarization and Inflammatory Responses in COPD.International journal of chronic obstructive pulmonary disease · 2026Article
- Naringenin Accelerates Diabetic Wound Healing via Regulating Macrophage M2 Polarization and Efferocytosis.Food science & nutrition · 2025Article
- rhCC16 Suppresses Cellular Senescence and Ameliorates COPD-Like Symptoms by Activating the AMPK/Sirt1-PGC-1-α-TFAM Pathway to Promote Mitochondrial Function.Journal of cellular and molecular medicine · 2025Article
- miR-335-5p Predicts Elevated Chronic Obstructive Pulmonary Disease (COPD) Susceptibility and Its Role in Human Bronchial Epithelial Cells Injury.International journal of chronic obstructive pulmonary disease · 2025Article
- Advances on the Role of Lung Macrophages in the Pathogenesis of Chronic Obstructive Pulmonary Disease in the Era of Single-Cell Genomics.International journal of medical sciences · 2025Review
- Metabolic reprogramming of macrophages in chronic obstructive pulmonary disease.Frontiers in immunology · 2025Review
- Article
- Quantitative proteomic analysis of circulating exosomes reveals the mechanism by which Triptolide protects against collagen-induced arthritis.Immunity, inflammation and disease · 2024Article
- Article
- Article
- Dexmedetomidine regulates exosomal miR-29b-3p from macrophages and alleviates septic myocardial injury by promoting autophagy in cardiomyocytes via targeting glycogen synthase kinase 3β.Burns & trauma · 2024Article
- Exosomes: efficient macrophage-related immunomodulators in chronic lung diseases.Frontiers in cell and developmental biology · 2024Review
- Lung cancer associated with combustion particles and fine particulate matter (PMBiochemical pharmacology · 2023Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Extracellular vesicles (EVs)-mediated epithelium-macrophage crosstalk has been proved to maintain lung homeostasis in cigarette smoke-induced lung diseases such as chronic obstructive pulmonary disease (COPD). In our previous study, we found that EVs derived from cigarette smoke extract (CSE) treated BEAS-2B promoted M1 macrophage polarization, which probably accelerated the development of inflammatory responses. Naringenin has been proved to suppress M1 macrophage polarization, but whether naringenin regulates macrophage polarization mediated by EVs has not been reported. In this study, we firstly found that EVs derived from naringenin and CSE co-treated BEAS-2B significantly inhibited the expression of CD86 and CD80 and the secretion of tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β, inducible nitric oxide synthase (iNOS), and IL-12 in macrophage induced by EVs derived from CSE-treated BEAS-2B. Further research revealed that naringenin downregulated BEAS-2B-derived EVs miR-21-3p which targeted phosphatase and tensin homolog deleted on chromosome ten/protein kinase B (PTEN/AKT) cascade in macrophages and then suppressed M1 macrophage polarization. Subsequent proteomics suggested that naringenin decreased BEAS-2B-derived EVs poly ADP-ribose polymerase (PARP)1 expression thereby suppressing M1 macrophage polarization probably. Our study provides novel pharmacological references for the mechanism of naringenin in the treatment of cigarette smoke-induced lung inflammatory diseases.
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