ArticleBritish journal of pharmacology2011
Rescuing iron-overloaded macrophages by conservative relocation of the accumulated metal.
Article in British journal of pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 34 citations in OpenAlex.
- Targeting chelatable iron as a therapeutic modality in Parkinson's disease.Antioxidants & redox signaling · 2014Trial
- Machine learning-assisted screening of small-molecule drugs for suppressing protein aggregation and ROS generation based on ECL and CV dual-mode signals amplified by DNA.Chemical science · 2026Article
- Activating Ferroptosis of M1 Macrophages: A Novel Mechanism of Asiaticoside Encapsuled in GelMA for Anti-Inflammation in Diabetic Wounds.Exploration (Beijing, China) · 2025Article
- Iron-loaded deferiprone can support full hemoglobinization of cultured red blood cells.Scientific reports · 2023Article
- Intracellular Iron Binding and Antioxidant Activity of Phytochelators.Biological trace element research · 2022Article
- Mechanistic Insights Expatiating the Redox-Active-Metal-Mediated Neuronal Degeneration in Parkinson's Disease.International journal of molecular sciences · 2022Review
- Recent Developments in Metal-Based Drugs and Chelating Agents for Neurodegenerative Diseases Treatments.International journal of molecular sciences · 2019Review
- Article
- Drug Repurposing in Parkinson's Disease.CNS drugs · 2018Review
- The Relevance of Iron in the Pathogenesis of Multiple System Atrophy: A Viewpoint.Journal of Alzheimer's disease : JAD · 2018Review
- Deferiprone Rescues Behavioral Deficits Induced by Mild Iron Exposure in a Mouse Model of Alpha-Synuclein Aggregation.Neuromolecular medicine · 2017Article
- Perspective: What Makes It So Difficult to Mitigate Worldwide Anemia Prevalence?Advances in nutrition (Bethesda, Md.) · 2017Review
- Cp/Heph mutant mice have iron-induced neurodegeneration diminished by deferiprone.Journal of neurochemistry · 2015Article
- The Fe-S cluster-containing NEET proteins mitoNEET and NAF-1 as chemotherapeutic targets in breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Cancer cells with irons in the fire.Free radical biology & medicine · 2015Review
- Iron at the interface of immunity and infection.Frontiers in pharmacology · 2014Review
- Labile iron in cells and body fluids: physiology, pathology, and pharmacology.Frontiers in pharmacology · 2014Review
- Regional siderosis: a new challenge for iron chelation therapy.Frontiers in pharmacology · 2013Review
- NAF-1 and mitoNEET are central to human breast cancer proliferation by maintaining mitochondrial homeostasis and promoting tumor growth.Proceedings of the National Academy of Sciences of the United States of America · 2013 · on this mapArticle
- On improvement in ejection fraction with iron chelation in thalassemia major and the risk of future heart failure.Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance · 2011Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeSystemic iron deficiency concomitant with macrophage iron retention is characteristic of iron-refractory anaemias associated with chronic disease. The systemic misdistribution of iron, which is further exacerbated by parenteral iron supplementation, is mainly attributable to iron retention exerted on resident macrophages by hepcidin-mediated down-regulation of the iron exporter ferroportin. We aimed at developing an experimental macrophage-based cell model that recapitulates pathophysiological features of iron misdistribution found in chronic disorders and use it as a screening platform for identifying agents with the potential for relocating the accumulated metal and restoring affected functions. EXPERIMENTAL APPROACH: A raw macrophage subline was selected as cell model of iron retention based on their capacity to take up polymeric iron or aged erythrocytes excessively, resulting in a demonstrable increase of cell labile iron pools and oxidative damage that are aggravated by hepcidin. KEY
resultsThis model provided a three-stage high throughput screening platform for identifying agents with the combined ability to: (i) scavenge cell iron and thereby rescue macrophage cells damaged by iron-overload; (ii) bypass the ferroportin blockade by conveying the scavenged iron to other iron-starved cells in co-culture via transferrin but (iii) without promoting utilization of the scavenged iron by intracellular pathogens. As test agents we used chelators in clinical practice and found the oral chelator deferiprone fulfilled essentially all of the three criteria. CONCLUSIONS AND IMPLICATIONS: We provide a proof of principle for conservative iron relocation as complementary therapeutic approach for correcting the misdistribution of iron associated with chronic disease and exacerbated by parenteral iron supplementation.
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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.