ArticleOncotarget2017
Reactive oxygen species levels control NF-κB activation by low dose deferasirox in erythroid progenitors of low risk myelodysplastic syndromes.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 37 citations in OpenAlex.
- A variant erythroferrone disrupts iron homeostasis inScience translational medicine · 2019Trial
- Deferasirox, an iron chelator, impacts myeloid differentiation by modulating NF-kB activity via mitochondrial ROS.British journal of haematology · 2024Article
- Time-dependent effects of hypoxia on cell metabolism, signaling, and iron homeostasis in the hematopoietic progenitor model KG1a.FEBS open bio · 2023Article
- Luspatercept (RAP-536) modulates oxidative stress without affecting mutation burden in myelodysplastic syndromes.Annals of hematology · 2022Article
- Review
- Emerging Roles of the Iron Chelators in Inflammation.International journal of molecular sciences · 2022Review
- Deferasirox-induced robust and dose-dependent reversal of anemia in a patient with variants in the TRIB2 and ABCB6 genes.Blood advances · 2022Article
- EnvIRONmental Aspects in Myelodysplastic Syndrome.International journal of molecular sciences · 2021Review
- Genome-wide transcriptomics leads to the identification of deregulated genes after deferasirox therapy in low-risk MDS patients.The pharmacogenomics journal · 2020Article
- Article
- Protein Carbonylation in Patients with Myelodysplastic Syndrome: An Opportunity for Deferasirox Therapy.Antioxidants (Basel, Switzerland) · 2019Article
- [Research progress of characteristics and mechanisms of iron overload affecting bone marrow hematopoiesis].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2019Article
- Atrial fibrillation in β-thalassemia patients with a focus on the role of iron-overload and oxidative stress: A review.Journal of cellular physiology · 2019Review
- Deferasirox drives ROS-mediated differentiation and induces interferon-stimulated gene expression in human healthy haematopoietic stem/progenitor cells and in leukemia cells.Stem cell research & therapy · 2019Article
- Dyserythropoiesis evaluated by the RED score and hepcidin:ferritin ratio predicts response to erythropoietin in lower-risk myelodysplastic syndromes.Haematologica · 2019Article
- Article
- Iron overload impairs normal hematopoietic stem and progenitor cells through reactive oxygen species and shortens survival in myelodysplastic syndrome mice.Haematologica · 2018Article
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Authors and funding
16 authors at 8 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anemia is a frequent cytopenia in myelodysplastic syndromes (MDS) and most patients require red blood cell transfusion resulting in iron overload (IO). Deferasirox (DFX) has become the standard treatment of IO in MDS and it displays positive effects on erythropoiesis. In low risk MDS samples, mechanisms improving erythropoiesis after DFX treatment remain unclear. Herein, we addressed this question by using liquid cultures with iron overload of erythroid precursors treated with low dose of DFX (3μM), which corresponds to DFX 5 mg/kg/day, an unusual dose used for iron chelation. We highlight a decreased apoptosis rate and an increased proportion of cycling cells, both leading to higher proliferation rates. The iron chelation properties of low dose DFX failed to activate the Iron Regulatory Proteins and to support iron depletion, but low dose DFX dampers intracellular reactive oxygen species. Furthermore low concentrations of DFX activate the NF-κB pathway in erythroid precursors triggering anti-apoptotic and anti-inflammatory signals. Establishing stable gene silencing of the Thioredoxin (TRX) 1 genes, a NF-κB modulator, showed that fine-tuning of reactive oxygen species (ROS) levels regulates NF-κB. These results justify a clinical trial proposing low dose DFX in MDS patients refractory to erythropoiesis stimulating agents.
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