ReviewAntioxidants (Basel, Switzerland)2021
The Role of RBC Oxidative Stress in Sickle Cell Disease: From the Molecular Basis to Pathologic Implications.
Review in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 2 of them syntheses that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
44 citing papers in PubMed, 2 syntheses or guidelines pooled it, 79 citations in OpenAlex.
- Oxidative Stress, Antioxidant Capacity, Dyslipidemia and Cardiovascular Risk in Sickle Cell Disease: A Systematic Review and Meta-Analysis.TheScientificWorldJournal · 2026Pooled it
- Antioxidant supplementation for sickle cell disease.The Cochrane database of systematic reviews · 2024Pooled it
- Antibody-Dependent and Antibody-Independent Hemolysis in Sickle Cell Disease.Antibodies (Basel, Switzerland) · 2026Review
- Thrombocytosis and the generation of platelet-derived microparticles in the pathophysiology of sickle cell disease.British journal of haematology · 2026Review
- Reactive Oxygen Species in Cardiovascular and Hematological Diseases: Mechanisms and Therapeutic Strategies.Cureus · 2026Review
- Repurposing Tyrosine Kinase Inhibitors for Sickle Cell Disease: Focus on Band 3 Phosphorylation.Biomedicines · 2026Review
- Redox Modulation of Erythropoiesis by Selenoproteins.Biological trace element research · 2026Review
- Review
- CRISPR-Cas9-mediated therapeutics: Current clinical trials and therapy approval landscape to treat human diseases.Molecular therapy. Nucleic acids · 2026Review
- Protein Arginine Methyltransferases in γ-Globin Regulation and Sickle Cell Disease: Emerging Connections to Oxidative Stress.Antioxidants (Basel, Switzerland) · 2026Review
- Unravelling the Immunological Enigma of Sickle Cell Disease: Current Understanding and Future Directions.Immunology · 2026Review
- Immunopathogenesis of Sickle Cell Disease: Mechanisms of Immune Dysregulation and Clinical Consequences, a Narrative Review.Journal of blood medicine · 2026Review
- Hemoglobin glycation index and short-term mortality in sepsis: a retrospective cohort study with external validation.Frontiers in medicine · 2026Article
- CRISPR editing of HPFH3 genotype induces γ-globin expression and reverses sickle cell disease and β-thalassemia phenotypes.Stem cell research & therapy · 2025Article
- Circulating miR-145-5p and miR-133a-3p in pediatric sickle cell disease: biomarker potential for vaso-occlusive crises and disease activity.Annals of hematology · 2025Article
- Small Molecule Regulation of Iron Homeostasis: Design and Optimization of Novel Iron Chelators Based on a Thiosemicarbazone Scaffold.Journal of molecular structure · 2025Article
- Hemoglobin S Promotes Glycemic Dysregulation in a Mouse Model of Human Sickle Cell Disease.Endocrinology · 2025Article
- Crosstalk Between Sickle Cell Disease and Ferroptosis.International journal of molecular sciences · 2025Review
- Assessment of Inter-Reader Reliability of Fazekas Scoring on Magnetic Resonance Imaging of the Brain in Adult Patients with Sickle Cell Disease.Diagnostics (Basel, Switzerland) · 2025Article
- Vitamin C: From Self-Sufficiency to Dietary Dependence in the Framework of Its Biological Functions and Medical Implications.Life (Basel, Switzerland) · 2025Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Sickle cell disease (SCD) is an inherited monogenic disorder and the most common severe hemoglobinopathy in the world. SCD is characterized by a point mutation in the β-globin gene, which results in hemoglobin (Hb) S production, leading to a variety of mechanistic and phenotypic changes within the sickle red blood cell (RBC). In SCD, the sickle RBCs are the root cause of the disease and they are a primary source of oxidative stress since sickle RBC redox state is compromised due to an imbalance between prooxidants and antioxidants. This imbalance in redox state is a result of a continuous production of reactive oxygen species (ROS) within the sickle RBC caused by the constant endogenous Hb autoxidation and NADPH oxidase activation, as well as by a deficiency in the antioxidant defense system. Accumulation of non-neutralized ROS within the sickle RBCs affects RBC membrane structure and function, leading to membrane integrity deficiency, low deformability, phosphatidylserine exposure, and release of micro-vesicles. These oxidative stress-associated RBC phenotypic modifications consequently evoke a myriad of physiological changes involved in multi-system manifestations. Thus, RBC oxidative stress in SCD can ultimately instigate major processes involved in organ damage. The critical role of the sickle RBC ROS production and its regulation in SCD pathophysiology are discussed here.
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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.