ReviewHematology. American Society of Hematology. Education Program2014
Iron age: novel targets for iron overload.
Review in Hematology. American Society of Hematology. Education Program, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Expression of the FAM132B Gene in Iranian Patients with Beta-Thalassemia.International journal of hematology-oncology and stem cell research · 2025Article
- Targeting macro- and micro-nutrient regulation of HNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Hepcidin gene polymorphisms and iron overload in β-thalassemia major patients refractory to iron chelating therapy.BMC medical genetics · 2020Article
- Ineffective Erythropoiesis: Anemia and Iron Overload.Hematology/oncology clinics of North America · 2018Review
- Emerging Therapies.Hematology/oncology clinics of North America · 2018Review
- What can we learn from ineffective erythropoiesis in thalassemia?Blood reviews · 2018Review
- Inhibition of heme oxygenase ameliorates anemia and reduces iron overload in a β-thalassemia mouse model.Blood · 2018Article
- The plasma membrane metal-ion transporter ZIP14 contributes to nontransferrin-bound iron uptake by human β-cells.American journal of physiology. Cell physiology · 2017Article
- Associations between Lifestyle Factors and Iron Overload in Korean Adults.Clinical nutrition research · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Excess iron deposition in vital organs is the main cause of morbidity and mortality in patients affected by β-thalassemia and hereditary hemochromatosis. In both disorders, inappropriately low levels of the liver hormone hepcidin are responsible for the increased iron absorption, leading to toxic iron accumulation in many organs. Several studies have shown that targeting iron absorption could be beneficial in reducing or preventing iron overload in these 2 disorders, with promising preclinical data. New approaches target Tmprss6, the main suppressor of hepcidin expression, or use minihepcidins, small peptide hepcidin agonists. Additional strategies in β-thalassemia are showing beneficial effects in ameliorating ineffective erythropoiesis and anemia. Due to the suppressive nature of the erythropoiesis on hepcidin expression, these approaches are also showing beneficial effects on iron metabolism. The goal of this review is to discuss the major factors controlling iron metabolism and erythropoiesis and to discuss potential novel therapeutic approaches to reduce or prevent iron overload in these 2 disorders and ameliorate anemia in β-thalassemia.
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What OpenQuestion holds
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.