ReviewBlood2024
Elevating fetal hemoglobin: recently discovered regulators and mechanisms.
Review in Blood, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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
19 citing papers in PubMed.
- Article
- CRISPR-Cas9 and precision editing technologies linking functional genomics to clinical translation in genetic diseases.Clinical and translational medicine · 2026Review
- UCA1 lncRNA regulates γ-globin expression by modulating the miR-148b/BCL11A axis.Life science alliance · 2026Article
- PGC-1α agonism via oral administration of ZLN005 induces fetal hemoglobin and is antisickling in sickle mice.Blood advances · 2026Article
- COUP-TFII regulates hemoglobin switching by activating the BCL11A-XL repressor LIN28B and directly binding δ and β globin promoters in fetalHaematologica · 2026Article
- β-Thalassemia Minor and Pregnancy Outcomes: Pathophysiology, Clinical Implications, and Management.Medical sciences (Basel, Switzerland) · 2026Review
- Complex HBB gene editing outcomes revealed by a fluorescent reporter cell model.Molecular therapy. Nucleic acids · 2026Article
- Placental iron utilisation in fetal growth restriction: alterations in mitochondrial haem synthesis and iron-sulphur cluster assembly pathways.The Journal of physiology · 2026Article
- Highly discriminative globin gene activation by the noncanonical BAF chromatin remodeling complex.Blood · 2026Article
- Changes in Fetal Hemoglobin in Very Preterm Infants Born Small for Gestational Age: A Retrospective Observational Study.Children (Basel, Switzerland) · 2026Article
- Comprehensive Review of Genetic and Epigenetic Regulation of Fetal Hemoglobin in β-Hemoglobinopathies: From Molecular Mechanisms to Clinical Applications.Mediterranean journal of hematology and infectious diseases · 2026Review
- Advances in the characterization of in vitro-generated red blood cells: from biophysical properties to functional applications.Stem cell research & therapy · 2025Review
- Systematic enhancer mapping and functional analysis in zebrafish with optimized CRISPR interference.Nucleic acids research · 2025Article
- Selective AMPKβ1 activation induces fetal hemoglobin in human erythroid cells and sickle cell mice via the noncanonical NRF2 pathway.Science advances · 2025Article
- Mechanisms of Globin Gene Regulation in Mammals.Annual review of genetics · 2025Review
- Genetic Engineering in Hematopoietic Stem Cells for β-Hemoglobinopathies Treatment: Advances, Challenges, and Clinical Translation.International journal of hematology-oncology and stem cell research · 2025Review
- HRI protein kinase in cytoplasmic heme sensing and mitochondrial stress response: Relevance to hematological and mitochondrial diseases.The Journal of biological chemistry · 2025Review
- RNA Editors Sculpt the Transcriptome During Terminal Erythropoiesis.Research square · 2025Article
- Nonclinical evaluation of HBG1/2 and BCL11A as genome-editing targets for the treatment of β-hemoglobinopathies.Blood advances · 2025Article
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.
Funding
Abstract
abstractIt has been known for over half a century that throughout ontogeny, humans produce different forms of hemoglobin, a tetramer of α- and β-like hemoglobin chains. The switch from fetal to adult hemoglobin occurs around the time of birth when erythropoiesis shifts from the fetal liver to the bone marrow. Naturally, diseases caused by defective adult β-globin genes, such as sickle cell disease and β-thalassemia, manifest themselves as the production of fetal hemoglobin fades. Reversal of this developmental switch has been a major goal to treat these diseases and has been a driving force to understand its underlying molecular biology. Several review articles have illustrated the long and at times arduous paths that led to the discovery of the first transcriptional regulators involved in this process. Here, we survey recent developments spurred by the discovery of CRISPR tools that enabled for the first time high-throughput genetic screens for new molecules that impact the fetal-to-adult hemoglobin switch. Numerous opportunities for therapeutic intervention have thus come to light, offering hope for effective pharmacologic intervention for patients for whom gene therapy is out of reach.
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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.