ArticlePediatric research2024
The association between growth differentiation factor-15, erythroferrone, and iron status in thalassemic patients.
Article in Pediatric research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Oral lactoferrin as a treatment of pediatrics' anemia resulted from chronic kidney diseases: a randomized controlled trial.Scientific reports · 2025Trial
- FPN1-8C>G Polymorphism as a potential genetic modifier of iron overload in transfusion-dependent β-Thalassemia major patients receiving HbF augmentation therapy.Pakistan journal of medical sciences · 2026Article
- Association of growth differentiation factor-15 with muscle wasting and anemia in chronic kidney disease.The journal of nutrition, health & aging · 2026Article
- Article
- Mechanism-Based Pharmacokinetic/Pharmacodynamic Modeling of Erythroferrone in Anemic Rats with Chronic Kidney Disease and Chemotherapy-Induced Anemia: An Early Biomarker for Hemoglobin Response and rHuEPO Hyporesponsiveness.ACS pharmacology & translational science · 2025Article
- Cardiac injury caused by iron overload in thalassemia.Frontiers in pediatrics · 2025Review
- Comprehensive expression of long non-coding RNAs and association with iron and erythropoiesis regulatory proteins in transfusion-dependent β-thalassemia.Archives of medical science : AMS · 2025Article
- Erythroferrone-Driven Regulation of Hepcidin and Iron Levels in Polytransfused Sickle Cell Anaemia Patients: A Prospective Study.BioMed research international · 2025Article
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4 authors at 1 institution in 1 country.
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Abstract
backgroundIron overload can result in grave consequences in thalassemic patients, despite the availability of iron chelators. Therefore, alternative pathways aiming to reduce iron toxicity are currently investigated. Among which, reduction of iron absorption through control of hepcidin production appears to be promising. In this study, we investigated growth differentiation factor-15 (GDF15) and erythroferrone (ERFE) as potential suppressors of hepcidin.
methodsThis cross-sectional study was conducted on 61 thalassemic patients and 60 healthy controls. The frequency of GDF15 gene polymorphism (rs4808793) (-3148C/G), serum level of GDF15 and erythroferrone were measured and correlated with those of hepcidin and serum ferritin.
resultsThe presence of GDF15 gene mutations were significantly higher in the patients' group compared to controls (P value 0.035). Also, thalassemia patients had significantly higher levels of GDF15 and ERFE and lower hepcidin levels than controls (P value < 0.001). Serum hepcidin level showed significantly negative correlations with GDF15, ERFE, reticulocyte count, LDH level, and serum ferritin. Contrarily, it had highly significant positive correlation with hemoglobin.
conclusionsHigh level of GDF15 and/or ERFE may inhibit hepcidin production and increase iron load in patients with thalassemia; therefore, medications that suppress their actions may provide new therapeutic potentials for iron toxicity. IMPACT: Iron overload continues to be a major contributor to high morbidity and mortality in patients with thalassemia. New strategies together with proper chelation, need to be developed to minimize the effect of iron toxicity. Growth differentiation factor-15 (GDF15) and erythroferrone (ERFE) inhibit hepcidin production and increase iron levels in conditions with ineffective erythropoiesis. Medications that suppress the production or interfere with the action of GDF15 or ERFE may represent new therapeutic potentials for iron toxicity. Prevention of iron toxicity will significantly reduce morbidity and mortality and improve the quality of life of thalassemia patients.
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