ArticleInternational journal of chronic obstructive pulmonary disease2025
Sputum SLC40A1 as a Novel Biomarker is Increased in Patients with Acute Exacerbation of Chronic Obstructive Pulmonary Disease.
Article in International journal of chronic obstructive pulmonary disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- METTL14 knockdown mitigates HG-induced HK-2 cell apoptosis, inflammation, and ferroptosis by promoting SLC40A1.European journal of medical research · 2026Article
- Ironing out COPD: ferroptosis-driven immune dysregulation, metabolic rewiring, and precision therapeutic opportunities.Frontiers in immunology · 2026Review
- SLC40A1 (iron transporter): mechanistic regulation, role in disease pathogenesis, and prospects for targeted therapy.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Solute carrier family 40 member 1 (SLC40A1 or Ferroportin) is a cell surface glycoprotein that participates in the efflux of cellular iron and disease pathogenesis. Induced sputum is a non-invasive method for lung sample collection. However, it remains unknown whether SLC40A1 is a potential diagnostic biomarker in induced sputum cells of patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD). We in this study aimed to investigate the expression and the anti-inflammatory role of SLC40A1 in the induced-sputum cells of AECOPD patients. Methods: A total of 35 induced sputum samples were collected from patients with AECOPD. Flow cytometry analysis was used to determine inflammatory cell phenotypes and SLC40A1 expression. Murine RAW 264.7 cell lines were treated with cigarette smoke extract (CSE) and SLC40A1-shRNA for SLC40A1 expression in vitro. ELISA was used for measurement of pro-inflammatory cytokine expression in vitro. Results: Flow cytometry analysis showed that sputum neutrophils were increased in AECOPD patients with 3-5 exacerbations per year compared to 1 exacerbation per year, accompanied by elevated expression of CD40 and SLC40A1 in macrophages. The lung function (FEV1%pred) was reduced with a higher COPD exacerbation rate. There was a negative correlation between the FEV1% predicted and sputum neutrophil count. Patients expressing high levels of SLC40A1 exhibited higher exacerbation rates. SLC40A1 expression levels positively correlated with sputum neutrophils and negatively correlated with predicted FEV1%. In addition, mechanical ventilation reduces sputum neutrophils and SLC40A1 expression, particularly in patients with a high exacerbation rate. Further analysis in RAW 264.7 macrophage cell lines showed that cigarette smoke extract (CSE) increased the expression of SLC40A1, TNF-α, IL-6 and IL-10 at a concentration-dependent manner. SLC40A1 knockdown increased the expression of TNF-α and IL-6 and reduced the expression of IL-10 in CSE-treated macrophages. Conclusion: SLC40A1 in sputum macrophages is increased and closely related to AECOPD severity, it would be a potential anti-inflammatory biomarker of patients with AECOPD.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.