SynthesisExpert review of hematology2015
A systematic review of known mechanisms of hydroxyurea-induced fetal hemoglobin for treatment of sickle cell disease.
Synthesis in Expert review of hematology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 5 of them syntheses 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
53 citing papers in PubMed, 5 syntheses or guidelines pooled it, 93 citations in OpenAlex.
- Impact of telehealth on hydroxyurea adherence and clinical outcomes in sickle cell disease management: A systematic review and meta-analysis.Journal of managed care & specialty pharmacy · 2026Pooled it
- Interventions for chronic kidney disease in people with sickle cell disease.The Cochrane database of systematic reviews · 2023Pooled it
- Interventions for preventing silent cerebral infarcts in people with sickle cell disease.The Cochrane database of systematic reviews · 2020Pooled it
- Interventions for chronic kidney disease in people with sickle cell disease.The Cochrane database of systematic reviews · 2017Pooled it
- Interventions for preventing silent cerebral infarcts in people with sickle cell disease.The Cochrane database of systematic reviews · 2017Pooled it
- BCL11A and HBS1L-MYB polymorphisms, in association with hydroxyurea and sex, modulate fetal hemoglobin levels in individuals with sickle cell anemia in the western region of Bahia, Brazil.Molecular biology reports · 2026Article
- Roxadustat induced fetal hemoglobin in anemic CKD patients: a dual-center real-world observational cohort study.BMC nephrology · 2026Observational
- Gynecologic and Reproductive Health in Patients with Sickle Cell Disease: Underrecognized Challenges and Care Management Opportunities.Journal of clinical medicine · 2026Review
- Pleiotropic Effects of Polymorphisms in theInternational journal of molecular sciences · 2025Article
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- Article
- Identifying and addressing underuse in hematologic care through systems-based hematology.Research and practice in thrombosis and haemostasis · 2025Review
- The induction effect of hydroxyurea and metformin on fetal globin in the K562 cell line.Molecular medicine (Cambridge, Mass.) · 2025Article
- Hydroxyurea for Malignant Pertussis in Critically Ill Children.Critical care explorations · 2025Article
- Impact of hydroxycarbamide treatment on the whole-blood transcriptome in sickle cell disease.British journal of haematology · 2025Article
- CYB5R3 T117S tempers fetal hemoglobin induction by hydroxyurea in patients with sickle cell disease.Blood advances · 2024Article
- Impaired microvascular function in patients with sickle cell anemia and leg ulcers improved with healing.British journal of haematology · 2024Article
- Review
- Cytomegalovirus viremia in an 11-year-old child with sickle cell disease manifested only with fever: a case report.Annals of medicine and surgery (2012) · 2023Article
- TheJournal of pediatric genetics · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
aimTo report on molecular mechanisms of fetal hemoglobin (HbF) induction by hydroxyurea (HU) for the treatment of sickle cell disease. STUDY
designSystematic review.
resultsStudies have provided consistent associations between genomic variations in HbF-promoting loci and variable HbF level in response to HU. Numerous signal transduction pathways have been implicated, through the identification of key genomic variants in BCL11A, HBS1L-MYB, SAR1 or XmnI polymorphism that predispose the response to the treatment, and signal transduction pathways that modulate γ-globin expression (cAMP/cGMP; Giα/c-Jun N-terminal kinase/Jun; methylation and miRNA). Three main molecular pathways have been reported: i) Epigenetic modifications, transcriptional events and signaling pathways involved in HU-mediated response, ii) Signaling pathways involving HU-mediated response and iii) Post-transcriptional pathways (regulation by miRNAs).
conclusionsThe complete picture of HU-mediated mechanisms of HbF production in Sickle Cell Disease remains elusive. Research on post-transcriptional mechanisms could lead to therapeutic targets that may minimize alterations to the cellular transcriptome.
Indexed as
Identifiers
What Socratic 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 Socratic graph.