ArticleInternational journal of chronic obstructive pulmonary disease2022
NCOA4-Mediated Ferroptosis in Bronchial Epithelial Cells Promotes Macrophage M2 Polarization in COPD Emphysema.
Article in International journal of chronic obstructive pulmonary disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.
- The molecular mechanism of ferroptosis and its role in COPD.Frontiers in medicine · 2022Pooled it
- Ferroptosis in e-cigarette aerosol-associated respiratory injury.Archives of toxicology · 2026Review
- The Iron Lung: Ferroptosis and Iron Regulation in Aging and Lung Diseases.Physiology (Bethesda, Md.) · 2026Review
- Ironing out COPD: ferroptosis-driven immune dysregulation, metabolic rewiring, and precision therapeutic opportunities.Frontiers in immunology · 2026Review
- The Emerging Role of METTL3 in Lung Diseases.International journal of molecular sciences · 2025Review
- Review
- A bibliometric analysis of macrophages associated with chronic obstructive pulmonary disease from 2005 to 2025.Journal of thoracic disease · 2025Article
- MTMR14 depletion aggravates intrapulmonary inflammation and emphysema in experimental COPD through activating macrophage M1 polarization.Respiratory research · 2025Article
- Integrating Single-Cell and Experimental Analyses Uncover Macrophage Ferroptosis Is a Key Event in the Development of Chronic Obstructive Pulmonary Disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- FSP1 Acts in Parallel with GPX4 to Inhibit Ferroptosis in Chronic Obstructive Pulmonary Disease.American journal of respiratory cell and molecular biology · 2025Article
- Based exploration of the diagnostic value of oxidative stress-related key genes in chronic obstructive pulmonary disease.Cell biology and toxicology · 2025Article
- Ferroptosis in Pulmonary Disease and Lung Cancer: Molecular Mechanisms, Crosstalk Regulation, and Therapeutic Strategies.MedComm · 2025Review
- PGAM5 Modulates Macrophage Polarization, Aggravating Inflammation in COPD via the NF-κB Pathway.International journal of chronic obstructive pulmonary disease · 2025Article
- SCGB1A1 as a Key Regulator of Splenic Immune Dysfunction in COPD: Insights From a Murine Model.International journal of chronic obstructive pulmonary disease · 2025Article
- Downregulation of NCOA4 expression indicates poor prognosis and promotes the progression of cholangiocarcinoma.PloS one · 2025Article
- TFR1 as a Biomarker of Pulmonary Fibrosis Development in COPD Patients.International journal of chronic obstructive pulmonary disease · 2025Article
- Metabolic reprogramming of macrophages in chronic obstructive pulmonary disease.Frontiers in immunology · 2025Review
- Identification of JNK-JUN-NCOA axis as a therapeutic target for macrophage ferroptosis in chronic apical periodontitis.International journal of medical sciences · 2025Article
- Immune cell regulatory networks in chronic obstructive pulmonary disease: mechanistic analysis from innate to adaptive immunity.Frontiers in immunology · 2025Review
- Autophagy-mediated ferroptosis is involved in development of severe acute pancreatitis.BMC gastroenterology · 2024Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Macrophage polarization plays an important role in the pathogenesis of COPD emphysema. Changes in macrophage polarization in COPD remain unclear, while polarization and ferroptosis are essential factors in its pathogenesis. Therefore, this study investigated the relationship between macrophage polarization and ferroptosis in COPD emphysema. Methods: We measured macrophage polarization and the levels of matrix metalloproteinases (MMPs) in the lung tissues of COPD patients and cigarette smoke (CS)-exposed mice. Flow cytometry was used to determine macrophage (THP-M cell) polarization changes. Ferroptosis was examined by FerroOrange, Perls' DAB, C11-BODIPY and 4-HNE staining. Nuclear receptor coactivator 4 (NCOA4) was measured in the lung tissues of COPD patients and CS-exposed mice by western blotting. A cell study was performed to confirm the regulatory effect of NCOA4 on macrophage polarization. Results: Increased M2 macrophages and MMP9 and MMP12 levels were observed in COPD patients, CS-exposed mice and THP-M cells cocultured with CS extract (CSE)-treated human bronchial epithelial (HBE) cells. Increased NCOA4 levels and ferroptosis were confirmed in COPD. Treatment with NCOA4 siRNA and the ferroptosis inhibitor ferrostatin-1 revealed an association between ferroptosis and M2 macrophages. These findings support a role for NCOA4, which induces an increase in M2 macrophages, in the pathogenesis of COPD emphysema. Conclusion: In our study, CS led to the dominance of the M2 phenotype in COPD. We identified NCOA4 as a regulator of M2 macrophages and emphysema by mediating ferroptosis, which offers a new direction for research into COPD diagnostics and treatment.
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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 Socratic graph.