ArticleExperimental hematology2019
MIR-144-mediated NRF2 gene silencing inhibits fetal hemoglobin expression in sickle cell disease.
Article in Experimental hematology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 51 citations in OpenAlex.
- The role of hydroxyurea in modulating miRNA expression in sickle cell disease: molecular mechanisms and therapeutic implications.Annals of hematology · 2026Review
- Cholesterol-conjugated miR-29b induces fetal haemoglobin expression via γ-globin promoter demethylation in the Townes mouse model for sickle cell anaemia.British journal of haematology · 2025Article
- Innovations in Drug Discovery for Sickle Cell Disease Targeting Oxidative Stress and NRF2 Activation-A Short Review.International journal of molecular sciences · 2025Review
- Clinical implications of miRNAs in erythropoiesis, anemia, and other hematological disorders.Molecular biology reports · 2024Review
- Potential Use of MicroRNA Technology in Thalassemia Therapy.Journal of clinical medicine research · 2024Review
- miR-214 aggravates oxidative stress in thalassemic erythroid cells by targeting ATF4.PloS one · 2024Article
- Bach1 inhibitor HPP-D mediates γ-globin gene activation in sickle erythroid progenitors.Blood cells, molecules & diseases · 2024Article
- From Stress to Sick(le) and Back Again-Oxidative/Antioxidant Mechanisms, Genetic Modulation, and Cerebrovascular Disease in Children with Sickle Cell Anemia.Antioxidants (Basel, Switzerland) · 2023Review
- The Complex Genetic and Epigenetic Regulation of the Nrf2 Pathways: A Review.Antioxidants (Basel, Switzerland) · 2023Review
- Role of microRNA in hydroxyurea mediated HbF induction in sickle cell anaemia patients.Scientific reports · 2023Article
- The BACH1 inhibitor ASP8731 inhibits inflammation and vaso-occlusion and induces fetal hemoglobin in sickle cell disease.Frontiers in medicine · 2023Article
- miRNA Expression Associated with HbF in Saudi Sickle Cell Anemia.Medicina (Kaunas, Lithuania) · 2022Article
- Targeting Genetic Modifiers of HBG Gene Expression in Sickle Cell Disease: The miRNA Option.Molecular diagnosis & therapy · 2022Review
- LncRNA OIP5-AS1 reduces renal epithelial cell apoptosis in cisplatin-induced AKI by regulating the miR-144-5p/PKM2 axis.Biomedical journal · 2022Article
- A Description of the Hemolytic Component in Sickle Leg Ulcer: The Role of Circulating miR-199a-5p, miR-144, and miR-126.Biomolecules · 2022Article
- MicroRNA29B induces fetal hemoglobinFrontiers in medicine · 2022Article
- Article
- The intricacies of NRF2 regulation in cancer.Seminars in cancer biology · 2021Review
- Exploring epigenetic and microRNA approaches for γ-globin gene regulation.Experimental biology and medicine (Maywood, N.J.) · 2021Review
- The Role of miRNAs as Therapeutic Tools in Sickle Cell Disease.Medicina (Kaunas, Lithuania) · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
Inherited genetic modifiers and pharmacologic agents that enhance fetal hemoglobin (HbF) expression reverse the clinical severity of sickle cell disease (SCD). Recent efforts to develop novel strategies of HbF induction include discovery of molecular targets that regulate γ-globin gene transcription and translation. The purpose of this study was to perform genome-wide microRNA (miRNA) analysis to identify genes associated with HbF expression in patients with SCD. We isolated RNA from purified reticulocytes for microarray-based miRNA expression profiling. Using samples from patients with contrasting HbF levels, we observed an eightfold upregulation of miR-144-3p (miR-144) and miR-144-5p in the low-HbF group compared with those with high HbF. Additional analysis by reverse transcription quantitative polymerase chain reaction confirmed individual miR-144 expression levels of subjects in the two groups. Subsequent functional studies in normal and sickle erythroid progenitors showed NRF2 gene silencing by miR-144 and concomitant repression of γ-globin transcription; by contrast, treatment with miR-144 antagomir reversed its silencing effects in a dose-dependent manner. Because NRF2 regulates reactive oxygen species levels, additional studies investigated mechanisms of HbF regulation using a hemin-induced oxidative stress model. Treatment of KU812 cells with hemin produced an increase in NRF2 expression and HbF induction that reversed with miR-144 pretreatment. Chromatin immunoprecipitation assay confirmed NRF2 binding to the γ-globin antioxidant response element, which was inhibited by miR-144 mimic treatment. The genome-wide miRNA microarray and primary erythroid progenitor data support a miR-144/NRF2-mediated mechanism of γ-globin gene regulation in SCD.
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.