ReviewBlood advances2019
Decoding the role of SOD2 in sickle cell disease.
Review in Blood advances, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 36 citations in OpenAlex.
- TWEAK/Fn14 Signaling Drives Oxidative Cardiac Injury in Systemic Lupus Erythematosus: Evidence From Patient Biomarker Studies, Lupus Mouse Models, and Cardiomyocyte Assays.Arthritis & rheumatology (Hoboken, N.J.) · 2026Article
- Acute hemolytic crises and clinical course in a Japanese family with Hb Santander: a detailed case report.International journal of hematology · 2025Article
- Targeting tumor metabolic flexibility enhances radiotherapeutic efficacy via mitochondrial complex I Inhibition in an intracranial S180 sarcoma mouse model.Scientific reports · 2025Article
- The involvement of mitochondria in erythrocyte pathology and diseases: from mechanisms to therapeutic strategies.Clinical and experimental medicine · 2025Review
- Crosstalk Between Sickle Cell Disease and Ferroptosis.International journal of molecular sciences · 2025Review
- Oral administration of aripiprazole to Drosophila causes intestinal toxicity.Disease models & mechanisms · 2025Article
- Deficiency of Caveolin-1 Aggravates Cardiac Infarction Injury by Disturbing the Endothelial Homeostasis.International journal of medical sciences · 2025Article
- Transcriptomic analysis of the effect of remote ischaemic conditioning in an animal model of necrotising enterocolitis.Scientific reports · 2024Article
- Sickle Cell Disease Update: New Treatments and Challenging Nutritional Interventions.Nutrients · 2024Review
- Ferroptosis as an emerging target in sickle cell disease.Current research in toxicology · 2024Article
- Circular RNAs: Promising Treatment Targets and Biomarkers of Ischemic Stroke.International journal of molecular sciences · 2023Review
- Flipping Off and On the Redox Switch in the Microcirculation.Annual review of physiology · 2023Review
- Mitochondria: Emerging Consequential in Sickle Cell Disease.Journal of clinical medicine · 2023Review
- Endogenous SOD2 (Superoxide Dismutase) Regulates Platelet-Dependent Thrombin Generation and Thrombosis During Aging.Arteriosclerosis, thrombosis, and vascular biology · 2023Article
- Article
- Role of Toll-like receptor 4 in intravascular hemolysis-mediated injury.The Journal of pathology · 2022Article
- Article
- A Viral Long Non-Coding RNA Protects against Cell Death during Human Cytomegalovirus Infection of CD14+ Monocytes.Viruses · 2022Article
- Endothelial superoxide dismutase 2 is decreased in sickle cell disease and regulates fibronectin processing.Function (Oxford, England) · 2022Article
- Impact of Superoxide Dismutase Genetic Polymorphism (SOD2 Val16Ala) and Superoxide Dismutase Level on Disease Severity in a Cohort of Egyptian Sickle Cell Disease Patients.Mediterranean journal of hematology and infectious diseases · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Sickle cell disease (SCD) is an inherited hemoglobinopathy caused by a single point mutation in the β-globin gene. As a consequence, deoxygenated hemoglobin polymerizes triggering red blood cell sickling and hemolysis, vaso-occlusion, and ischemia/reperfusion. Allied to these pathologies is the overproduction of reactive oxygen species driven by hemoglobin Fenton chemistry and peroxidase reactions as well as by secondary activation of vascular oxidases, including NAD(P)H oxidase and xanthine oxidase. In addition, hypoxia, produced by sickle red blood cell occlusion, disrupts mitochondrial metabolism and generates excess superoxide through electron leak from the mitochondrial respiratory chain. Superoxide dismutase 2 (SOD2) is a mitochondrial-specific antioxidant enzyme that dismutates superoxide to hydrogen peroxide, which is then converted to water by catalase and glutathione peroxidase. In SCD, the antioxidant defense system is significantly diminished through decreased expression and activity levels of antioxidant enzymes, including superoxide dismutase, catalase, and glutathione peroxidase. From a translational perspective, genetic variants including a missense variant in SOD2 (valine to alanine at position 16) are present in 45% of people with African ancestry and are associated with increased sickle complications. While it is known that there is an imbalance between oxidative species and antioxidant defenses in SCD, much more investigation is warranted. This review summarizes our current understanding of antioxidant defense systems in SCD, particularly focused on SOD2, and provides insight into challenges and opportunities as the field moves forward.
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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.