ArticleAmerican journal of physiology. Lung cellular and molecular physiology2021
MiR-223 is increased in lungs of patients with COPD and modulates cigarette smoke-induced pulmonary inflammation.
Article in American journal of physiology. Lung cellular and molecular physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.
- Animal models of chronic obstructive pulmonary disease: a systematic review.Frontiers in medicine · 2024Pooled it
- miR-766-5p Attenuates Cigarette Smoke-Induced COPD by Targeting MAPK1.Journal of biochemical and molecular toxicology · 2026Article
- Diagnostic and Monitoring Potential of Sputum-Derived miRNAs in Patients with Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2026Review
- Clinical role of miR-1271-5p in severe pediatric pneumonia and its prognostic value.BMC immunology · 2026Article
- Sputum Exosomal microRNAs as Non-Invasive Biomarkers in COPD: A Cross-Sectional Study.Biomedicines · 2025Article
- Association of miR-223-3p and miR-223-5p gene expression with levels of IgE, vitamin D and Mg+2 in pediatric asthma patients.Journal of medical biochemistry · 2025Article
- Functional validation to explore the protective role of miR-223 in Staphylococcus aureus-induced bovine mastitis.Journal of animal science and biotechnology · 2025Article
- miRNA Signatures in Alveolar Macrophages Related to Cigarette Smoke: Assessment and Bioinformatics Analysis.International journal of molecular sciences · 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
- Increasing serum miR-223-3p indicates the onset, severe development, and adverse prognosis of bronchiectasis: a retrospective study.BMC pulmonary medicine · 2024Article
- Alveolar Organoids in Lung Disease Modeling.Biomolecules · 2024Review
- Protection against cigarette smoke-induced chronic obstructive pulmonary disease via activation of the SIRT1/FoxO1 axis by targeting microRNA-132.American journal of translational research · 2024Article
- Soluble epoxide hydrolase deficiency attenuates airway inflammation in COPD via IRE1α/JNK/AP-1 signaling pathway.Journal of inflammation (London, England) · 2023Article
- Advanced models for respiratory disease and drug studies.Medicinal research reviews · 2023Review
- Changes and Clinical Value of Serum miR-24 and miR-223 Levels in Patients with Severe Pneumonia.International journal of general medicine · 2023Article
- lncRNA GAS5 promotes pyroptosis in COPD by functioning as a ceRNA to regulate the miR‑223‑3p/NLRP3 axis.Molecular medicine reports · 2022Article
- Review
- Seven ferroptosis-specific expressed genes are considered as potential biomarkers for the diagnosis and treatment of cigarette smoke-induced chronic obstructive pulmonary disease.Annals of translational medicine · 2022Article
- The Regulatory Role of MicroRNAs on Phagocytes: A Potential Therapeutic Target for Chronic Diseases.Frontiers in immunology · 2022Review
- Tweaking lung inflammation in COPD: the "mirky" ways of miRNAs.American journal of physiology. Lung cellular and molecular physiology · 2021Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Since microRNA (miR)-223-3p modulates inflammatory responses and chronic obstructive pulmonary disease (COPD) is associated with amplified pulmonary inflammation, we hypothesized that miR-223-3p plays a role in COPD pathogenesis. Expression of miR-223-3p was measured in lung tissue of two independent cohorts with patients with GOLD stage II-IV COPD, never smokers, and smokers without COPD. The functional role of miR-223-3p was studied in deficient mice and on overexpression in airway epithelial cells from COPD and controls. We observed higher miR-223-3p levels in patients with COPD stage II-IV compared with (non)-smoking controls, and levels were associated with higher neutrophil numbers in bronchial biopsies of patients with COPD. MiR-223-3p expression was also increased in lungs and bronchoalveolar lavage of cigarette smoke (CS)-exposed mice. CS-induced neutrophil and monocyte lung infiltration was stronger in miR-223-deficient mice on acute (5 days) exposure, but attenuated on subchronic (4 wk) exposure. Additionally, miR-223 deficiency attenuated acute and subchronic CS-induced lung infiltration of dendritic cells and T lymphocytes. Finally, in vitro overexpression of miR-223-3p in non-COPD airway epithelial cells suppressed C-X-C motif chemokine ligand 8 (CXCL8) and granulocyte monocyte-colony stimulation factor (GM-CSF) secretion and gene expression of the proinflammatory transcription factor
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