ReviewHematology/oncology clinics of North America2010
Anemia, ineffective erythropoiesis, and hepcidin: interacting factors in abnormal iron metabolism leading to iron overload in β-thalassemia.
Review in Hematology/oncology clinics of North America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 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
46 citing papers in PubMed, 95 citations in OpenAlex.
- Trial
- Sotatercept, a novel transforming growth factor β ligand trap, improves anemia in β-thalassemia: a phase II, open-label, dose-finding study.Haematologica · 2019Trial
- Iron overload across the spectrum of non-transfusion-dependent thalassaemias: role of erythropoiesis, splenectomy and transfusions.British journal of haematology · 2017Trial
- Deferasirox demonstrates a dose-dependent reduction in liver iron concentration and consistent efficacy across subgroups of non-transfusion-dependent thalassemia patients.American journal of hematology · 2013Trial
- Elevated liver iron concentration is a marker of increased morbidity in patients with β thalassemia intermedia.Haematologica · 2011Trial
- Postpartum Atypical Hemolytic Uremic Syndrome Complicating β-Thalassemia Intermedia: A Case Report and Literature Review.Journal of clinical medicine · 2026Article
- Pancreatic Volume in Thalassemia: Determinants and Association with Alterations of Glucose Metabolism.Diagnostics (Basel, Switzerland) · 2025Article
- Cardiac Dysfunction in β-Thalassemia: A Narrative Review.Research in heart yield and translational medicine · 2025Review
- Dysregulation of Ceruloplasmin, α2-Macroglobulin, and Alpha-2-HS-Glycoprotein in Transfusion-Dependent Thalassemia.Advances in hematology · 2025Article
- Cardiac injury caused by iron overload in thalassemia.Frontiers in pediatrics · 2025Review
- Mechanism and application prospect of ferroptosis inhibitors in improving osteoporosis.Frontiers in endocrinology · 2024Review
- Heme oxygenase 1 in erythropoiesis: an important regulator beyond catalyzing heme catabolism.Annals of hematology · 2023Review
- Prime Editor 3 Mediated Beta-Thalassemia Mutations of theInternational journal of molecular sciences · 2022Article
- Host and microbiota derived extracellular vesicles: Crucial players in iron homeostasis.Frontiers in medicine · 2022Review
- The hepatic extramedullary hematopoiesis during experimental murineFrontiers in immunology · 2022Article
- Review
- Abnormal regulation of microRNAs and related genes in pediatric β-thalassemia.Journal of clinical laboratory analysis · 2021Article
- Iron Status in Newly DiagnosedBioMed research international · 2021Article
- The mechanisms of pathological extramedullary hematopoiesis in diseases.Cellular and molecular life sciences : CMLS · 2020Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
β-Thalassemia is a genetic disorder caused by mutations in the β-globin gene and characterized by chronic anemia caused by ineffective erythropoiesis, and accompanied by a variety of serious secondary complications such as extramedullary hematopoiesis, splenomegaly, and iron overload. In the past few years, numerous studies have shown that such secondary disease conditions have a genetic basis caused by the abnormal expression of genes with a role in controlling erythropoiesis and iron metabolism. In this article, the most recent discoveries related to the mechanism(s) responsible for anemia/ineffective erythropoiesis and iron overload are discussed in detail. Particular attention is paid to the pathway(s) controlling the expression of hepcidin, which is the main regulator of iron metabolism, and the Epo/EpoR/Jak2/Stat5 signaling pathway, which regulates erythropoiesis. Better understanding of how these pathways function and are altered in β-thalassemia has revealed several possibilities for development of new therapeutic approaches to treat of the complications of this disease.
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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.