ArticleThe Journal of biological chemistry2015
Intestine-specific Disruption of Hypoxia-inducible Factor (HIF)-2α Improves Anemia in Sickle Cell Disease.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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.
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Who cites it
32 citing papers in PubMed, 44 citations in OpenAlex.
- Hepatic Enzyme Abnormalities and Their Association With Hematological Parameters in Sickle Cell Disease: A Case-Control Study in Cameroon.Health science reports · 2026Article
- Uric Acid Induces Hepatocytes Ferroptosis Through HIF-2α/DMT1-Mediated Iron Overload.International journal of molecular sciences · 2026Article
- Iron and the Intestinal Microbiome.Advances in experimental medicine and biology · 2025Review
- Effects of breast-fed infants-derivediScience · 2024Article
- Activation of Intestinal HIF2α Ameliorates Iron-Refractory Anemia.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Mechanisms controlling cellular and systemic iron homeostasis.Nature reviews. Molecular cell biology · 2024Review
- Relationships Between Markers of Iron Status and Hematological Parameters in Patients With Sickle Cell Disease.Advances in hematology · 2024Article
- The iron chaperone poly(rC)-binding protein 1 regulates iron efflux through intestinal ferroportin in mice.Blood · 2023Article
- High-Altitude Hypoxia Induces Excessive Erythrocytosis in Mice via Upregulation of the IntestinalBiomedicines · 2023Article
- Novel lentiviral vectors for gene therapy of sickle cell disease combining gene addition and gene silencing strategies.Molecular therapy. Nucleic acids · 2023Article
- TMPRSS6 as a Therapeutic Target for Disorders of Erythropoiesis and Iron Homeostasis.Advances in therapy · 2023Review
- (De)ironing out sickle cell disease.Blood · 2023Article
- Dietary iron restriction protects against vaso-occlusion and organ damage in murine sickle cell disease.Blood · 2023Article
- Probiotic Consortia and Their Metabolites Ameliorate the Symptoms of Inflammatory Bowel Diseases in a Colitis Mouse Model.Microbiology spectrum · 2022Article
- Isn't it ironic: better RBCs by blocking iron.Blood · 2022Article
- The oral ferroportin inhibitor vamifeport improves hemodynamics in a mouse model of sickle cell disease.Blood · 2022Article
- Review
- Revisiting anemia in sickle cell disease and finding the balance with therapeutic approaches.Blood · 2022Article
- Article
- Oxygen-sensing mechanisms in development and tissue repair.Development (Cambridge, England) · 2021Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Sickle cell disease (SCD) is caused by genetic defects in the β-globin chain. SCD is a frequently inherited blood disorder, and sickle cell anemia is a common type of hemoglobinopathy. During anemia, the hypoxic response via the transcription factor hypoxia-inducible factor (HIF)-2α is highly activated in the intestine and is essential in iron absorption. Intestinal disruption of HIF-2α protects against tissue iron accumulation in iron overload anemias. However, the role of intestinal HIF-2α in regulating anemia in SCD is currently not known. Here we show that in mouse models of SCD, disruption of intestinal HIF-2α significantly decreased tissue iron accumulation. This was attributed to a decrease in intestinal iron absorptive genes, which were highly induced in a mouse model of SCD. Interestingly, disruption of intestinal HIF-2α led to a robust improvement in anemia with an increase in RBC, hemoglobin, and hematocrit. This was attributed to improvement in RBC survival, hemolysis, and insufficient erythropoiesis, which is evident from a significant decrease in serum bilirubin, reticulocyte counts, and serum erythropoietin following intestinal HIF-2α disruption. These data suggest that targeting intestinal HIF-2α has a significant therapeutic potential in SCD pathophysiology.
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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.