ReviewBlood2012
Reawakening fetal hemoglobin: prospects for new therapies for the β-globin disorders.
Review in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
101 citing papers in PubMed, 1 synthesis or guideline pooled it, 172 citations in OpenAlex.
- Hydroxyurea for reducing blood transfusion in non-transfusion dependent beta thalassaemias.The Cochrane database of systematic reviews · 2016Pooled it
- A phase 2 study of HQK-1001, an oral fetal haemoglobin inducer, in β-thalassaemia intermedia.British journal of haematology · 2014Trial
- UCA1 lncRNA regulates γ-globin expression by modulating the miR-148b/BCL11A axis.Life science alliance · 2026Article
- Sickle Cell Disease: From Ancient Origins to Modern Breakthroughs in Gene Therapy.Biomedicines · 2026Review
- New Gene Therapy Strategy for β-Thalassemia.Stem cell reviews and reports · 2026Review
- The Role of Hemoglobin in Temporomandibular Joint Osteoarthritis and the Therapeutic Potential of Hydroxyurea.International journal of dentistry · 2026Article
- MAZ regulates fetal hemoglobin repression by activating MYB transcription.Scientific reports · 2025Article
- Mechanisms of Globin Gene Regulation in Mammals.Annual review of genetics · 2025Review
- Unraveling the Mystery of Hemoglobin in Hypoxia-Accelerated Neurodegenerative Diseases.Biomolecules · 2025Review
- Total ginsenosides enhance γ-globin expression and fetal hemoglobin production in β-thalassemia models.Frontiers in pharmacology · 2025Article
- Genetic Modifiers of Hemoglobin Expression from a Clinical Perspective in Hemoglobinopathy Patients with Beta Thalassemia and Sickle Cell Disease.International journal of molecular sciences · 2024Review
- Emerging roles of SIRT1 activator, SRT2104, in disease treatment.Scientific reports · 2024Review
- Serum visfatin level in β-thalassemia and its correlation with disease severity.Journal of medicine and life · 2024Article
- Article
- Review
- Identification of a genomic DNA sequence that quantitatively modulates KLF1 transcription factor expression in differentiating human hematopoietic cells.Scientific reports · 2023Article
- Molecular Basis and Genetic Modifiers of Thalassemia.Hematology/oncology clinics of North America · 2023Review
- Automated Good Manufacturing Practice-Compatible CRISPR-Cas9 Editing of Hematopoietic Stem and Progenitor Cells for Clinical Treatment of β-Hemoglobinopathies.The CRISPR journal · 2023Article
- A specific G9a inhibitor unveils BGLT3 lncRNA as a universal mediator of chemically induced fetal globin gene expression.Nature communications · 2023Article
- Review
41 more citing papers are in PubMed but not listed here.
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 2 institutions in 1 country.
Funding
Abstract
The level of fetal hemoglobin (HbF) modifies the severity of the common β-globin disorders. Knowledge of the normal mechanisms that repress HbF in the adult stage has remained limited until recently despite nearly 3 decades of molecular investigation, in part because of imperfect model systems. Recent studies have provided new insights into the developmental regulation of globin genes and identified specific transcription factors and epigenetic regulators responsible for physiologic silencing of HbF. Most prominent among these regulators is BCL11A, a transcriptional repressor that inhibits adult-stage HbF expression. KLF1 and c-Myb are additional critical HbF-regulating erythroid transcription factors more broadly involved in erythroid gene expression programs. Chromatin modifiers, including histone deacetylases and DNA methyltransferases, also play key roles in orchestrating appropriate globin gene expression. Taken together, these discoveries present novel therapeutic targets for further consideration. Although substantial hurdles remain, opportunities are now rich for the rational design of HbF inducers.
Indexed as
Identifiers
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.