ArticleScientific reports2018
The Hepcidin/Ferroportin axis modulates proliferation of pulmonary artery smooth muscle cells.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 43 citations in OpenAlex.
- Iron Compartmentalisation and Vascular Endothelial Cell Dysfunction.Antioxidants (Basel, Switzerland) · 2026Review
- The Interplay Between IL-6, Hepcidin, and BMPR2 Signalling in Pulmonary Arterial Hypertension: Mechanistic Insights Into Vascular Remodelling.Pulmonary circulation · 2026Article
- Analysis of In Silico Properties and In Vitro Immunomodulatory Effects of Seven Synthetic Host Defence Peptides in Gilthead Seabream (Sparus aurata) Leucocytes.Marine biotechnology (New York, N.Y.) · 2025Article
- Intravenous iron treatment fuels chronic kidney disease-induced arterial media calcification in rats.The Journal of pathology · 2025Article
- The hepcidin-ferroportin axis influences mitochondrial function, proliferation, and migration in pulmonary artery endothelial and smooth muscle cells.Pulmonary circulation · 2024Article
- Article
- Effect of iron administration on the aortic iron content and vascular calcification in phosphorus-loaded chronic kidney disease rats.BMC nephrology · 2023Article
- Interleukin-6 and pulmonary hypertension: from physiopathology to therapy.Frontiers in immunology · 2023Review
- Human pulmonary artery endothelial cells upregulate ACE2 expression in response to iron-regulatory elements: Potential implications for SARS-CoV-2 infection.Pulmonary circulation · 2022Article
- Role of Pyroptosis and Ferroptosis in the Progression of Atherosclerotic Plaques.Frontiers in cell and developmental biology · 2022Review
- From Iron Metabolism to Ferroptosis: Pathologic Changes in Coronary Heart Disease.Oxidative medicine and cellular longevity · 2022Review
- Biological heterogeneity in idiopathic pulmonary arterial hypertension identified through unsupervised transcriptomic profiling of whole blood.Nature communications · 2021Article
- Non-Transferrin-Bound Iron in the Spotlight: Novel Mechanistic Insights into the Vasculotoxic and Atherosclerotic Effect of Iron.Antioxidants & redox signaling · 2021Review
- In silico analysis suggests disruption of interactions between HAMP from hepatocytes and SLC40A1 from macrophages in hepatocellular carcinoma.BMC medical genomics · 2021Article
- Nutritional immunity: the impact of metals on lung immune cells and the airway microbiome during chronic respiratory disease.Respiratory research · 2021Review
- Intravenous iron therapy and the cardiovascular system: risks and benefits.Clinical kidney journal · 2021Review
- Colocalization of Erythrocytes and Vascular Calcification in Human Atherosclerosis: A Systematic Histomorphometric Analysis.TH open : companion journal to thrombosis and haemostasis · 2021Article
- Review
- Iron in Cardiovascular Disease: Challenges and Potentials.Frontiers in cardiovascular medicine · 2021Review
- Investigation of CD26, a potential SARS-CoV-2 receptor, as a biomarker of age and pathology.Bioscience reports · 2020Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Studies were undertaken to examine any role for the hepcidin/ferroportin axis in proliferative responses of human pulmonary artery smooth muscle cells (hPASMCs). Entirely novel findings have demonstrated the presence of ferroportin in hPASMCs. Hepcidin treatment caused increased proliferation of these cells most likely by binding ferroportin resulting in internalisation and cellular iron retention. Cellular iron content increased with hepcidin treatment. Stabilisation of ferroportin expression and activity via intervention with the therapeutic monoclonal antibody LY2928057 reversed proliferation and cellular iron accumulation. Additionally, IL-6 treatment was found to enhance proliferation and iron accumulation in hPASMCs; intervention with LY2928057 prevented this response. IL-6 was also found to increase hepcidin transcription and release from hPASMCs suggesting a potential autocrine response. Hepcidin or IL-6 mediated iron accumulation contributes to proliferation in hPASMCs; ferroportin mediated cellular iron excretion limits proliferation. Haemoglobin also caused proliferation of hPASMCs; in other novel findings, CD163, the haemoglobin/haptoglobin receptor, was found on these cells and offers a means for cellular uptake of iron via haemoglobin. Il-6 was also found to modulate CD163 on these cells. These data contribute to a better understanding of how disrupted iron homeostasis may induce vascular remodelling, such as in pulmonary arterial hypertension.
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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.