ArticleJournal of immunology (Baltimore, Md. : 1950)2020
Hepcidin Is Essential for Alveolar Macrophage Function and Is Disrupted by Smoke in a Murine Chronic Obstructive Pulmonary Disease Model.
Article in Journal of immunology (Baltimore, Md. : 1950), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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.
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Who cites it
18 citing papers in PubMed, 22 citations in OpenAlex.
- Could Hepcidin Be a Phenotype-Related Biomarker in Patients with Stable Bronchiectasis?Life (Basel, Switzerland) · 2026Article
- Prognostic Relevance of Erythropoiesis-Stimulating Agent Dose Requirements in PIVOTAL and Its Implications for the Potential Mechanisms of Intravenous Iron Benefit in Maintenance Haemodialysis Patients.American journal of nephrology · 2026Article
- Iron and the lung: emerging roles of iron metabolism in pulmonary disease pathogenesis and therapy.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Review
- The Relationship Between Hepcidin and the Severity of Obstructive Sleep Apnea Syndrome and Obesity.Life (Basel, Switzerland) · 2026Article
- Effect of I Quit Ordinary Smoking (IQOS) Use on Hepcidin and Iron Parameters in Comparison with Conventional Smoking.Iranian journal of public health · 2025Article
- Extracellular iron and the lung microbiome in smoking and COPD.ERJ open research · 2025Article
- Hepcidin and Tissue-Specific Iron Regulatory Networks.Advances in experimental medicine and biology · 2025Review
- Could Hepcidin Be a New Biomarker in Patients with Idiopathic Pulmonary Fibrosis (IPF)?Journal of clinical medicine · 2024Article
- Transcriptomic analysis reveals distinct effects of cigarette smoke on murine airspace and bone-marrow derived macrophages.Respiratory research · 2024Article
- Iron deficiency and supplementation in heart failure.Nature reviews. Cardiology · 2024Review
- Recent evidence from omic analysis for redox signalling and mitochondrial oxidative stress in COPD.Journal of inflammation (London, England) · 2022Review
- Oxidative Stress in Chronic Obstructive Pulmonary Disease.Antioxidants (Basel, Switzerland) · 2022Review
- Red Blood Cell-Derived Iron Alters Macrophage Function in COPD.Biomedicines · 2021Article
- Casting Iron in the Pathogenesis of Fibrotic Lung Disease.American journal of respiratory cell and molecular biology · 2021Article
- Nutritional immunity: the impact of metals on lung immune cells and the airway microbiome during chronic respiratory disease.Respiratory research · 2021Review
- Iron Availability in Tissue Microenvironment: The Key Role of Ferroportin.International journal of molecular sciences · 2021Review
- COVID-19 and iron dysregulation: distant sequence similarity between hepcidin and the novel coronavirus spike glycoprotein.Biology direct · 2020Article
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 4 countries.
Funding
Abstract
Chronic obstructive pulmonary disease (COPD) is a debilitating lung disease associated with cigarette smoking. Alterations in local lung and systemic iron regulation are associated with disease progression and pathogenesis. Hepcidin, an iron regulatory peptide hormone, is altered in subjects with COPD; however, the molecular role of hepcidin in COPD pathogenesis remains to be determined. In this study, using a murine model of smoke-induced COPD, we demonstrate that lung and circulating hepcidin levels are inhibited by cigarette smoke. We show that cigarette smoke exposure increases erythropoietin and bone marrow-derived erythroferrone and leads to expanded but inefficient erythropoiesis in murine bone marrow and an increase in ferroportin on alveolar macrophages (AMs). AMs from smokers and subjects with COPD display increased expression of ferroportin as well as hepcidin. Notably, murine AMs exposed to smoke fail to increase hepcidin in response to Gram-negative or Gram-positive infection. Loss of hepcidin in vivo results in blunted functional responses of AMs and exaggerated responses to
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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.