ArticleEBioMedicine2017
Disruption of the Hepcidin/Ferroportin Regulatory System Causes Pulmonary Iron Overload and Restrictive Lung Disease.
Article in EBioMedicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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.
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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
38 citing papers in PubMed, 61 citations in OpenAlex.
- Hepcidin as a Biomarker of Response to Antifibrotic Therapy in Idiopathic Pulmonary Fibrosis.Journal of clinical medicine · 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
- Downregulation of SLC40A1 leads to iron accumulation in fibrotic lung fibroblasts.Respiratory research · 2026Article
- The interplay of ferroptosis and oxidative stress in pulmonary fibrosis: from mechanisms to treatment.Frontiers in cell and developmental biology · 2026Review
- Influence of TMPRSS6 genotype on iron status parameters in stable COPD patients.Journal of medical biochemistry · 2025Article
- Ferroptosis in pulmonary fibrosis: pathogenesis and traditional Chinese medicine-driven therapeutic approaches.Frontiers in cell and developmental biology · 2025Review
- Nutritional insights into pulmonary fibrosis: a comprehensive review on the impact of vitamins.Frontiers in nutrition · 2025Review
- Longitudinal microcomputed tomography detects onset and progression of pulmonary fibrosis in conditionalAmerican journal of physiology. Lung cellular and molecular physiology · 2024Article
- Effect of iron administration on the aortic iron content and vascular calcification in phosphorus-loaded chronic kidney disease rats.BMC nephrology · 2023Article
- Protein Susceptibility to Peroxidation by 4-Hydroxynonenal in Hereditary Hemochromatosis.International journal of molecular sciences · 2023Article
- Ferroptosis in pulmonary fibrosis: an emerging therapeutic target.Frontiers in physiology · 2023Review
- Computational Modeling of Macrophage Iron Sequestration during Host Defense against Aspergillus.mSphere · 2022Article
- Role of Iron in Aging Related Diseases.Antioxidants (Basel, Switzerland) · 2022Article
- Non-heme iron overload impairs monocyte to macrophage differentiationFrontiers in immunology · 2022Article
- Investigating the Links between Lower Iron Status in Pregnancy and Respiratory Disease in Offspring Using Murine Models.Nutrients · 2021Article
- The Macrophage Iron Signature in Health and Disease.International journal of molecular sciences · 2021Review
- Casting Iron in the Pathogenesis of Fibrotic Lung Disease.American journal of respiratory cell and molecular biology · 2021Article
- The EHA Research Roadmap: Anemias.HemaSphere · 2021Article
- Nutritional immunity: the impact of metals on lung immune cells and the airway microbiome during chronic respiratory disease.Respiratory research · 2021Review
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Emerging evidence suggests that pulmonary iron accumulation is implicated in a spectrum of chronic lung diseases. However, the mechanism(s) involved in pulmonary iron deposition and its role in the in vivo pathogenesis of lung diseases remains unknown. Here we show that a point mutation in the murine ferroportin gene, which causes hereditary hemochromatosis type 4 (Slc40a1
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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.