The role of oxidant injury in the pathophysiology of human thalassemias
Open accessAbstract
The anemia in beta-thalassemia major is caused by a combination of hemolysis and ineffective erythropoiesis, with the latter being more important. Studies of the underlying cause of the hemolysis have indicated that oxidant injury to circulating red blood cells (RBCs) was of critical importance, with evidence of oxidant damage to RBC membrane proteins 4.1 and band 3. Therefore, it seemed reasonable that oxidant damage to thalassemic erythroid precursors would cause their accelerated apoptosis and ineffective erythropoiesis. However, direct analysis showed that the apoptotic programs turned on in thalassemics were not those triggered by oxidative damage but were dependent on activation of FAS/FAS-Ligand interaction. Thus, destruction of thalassemic erythroid precursors may involve different mechanisms from those that cause RBC hemolysis.
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Malfunction of antioxidant defense and/or conditions of increased oxidant production have severe consequences for RBCs on a subcellular level.
“Malfunction of antioxidant defense and/or conditions of increased oxidant production have severe consequences for RBCs on a subcellular level.”
From Red Blood Cell Function and Dysfunction: Redox Regulation, Nitric Oxide Metabolism, Anemia (2017) · cites this paper as [162]
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Cites
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The Evolution of Iron Chelators for the Treatment of Iron Overload Disease and Cancer
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Red Blood Cell Function and Dysfunction: Redox Regulation, Nitric Oxide Metabolism, Anemia
Kuhn, V., Diederich, L., Keller, T. C. S., Kramer, C. M., Lückstädt, W., Panknin, C., Suvorava, T., Isakson, B. E., Kelm, M., & Cortese-Krott, M. M. (2017) · Antioxidants & Redox Signaling · doi:10.1089/ars.2016.6954 · Cited by 469 · see citing works
- Authors
- Schrier, S. L., Centis, F., Verneris, M., Ma, L., & Angelucci, E.
- Affiliations
- San Salvatore Hospital (IT)
- Venue
- Redox Report
- Publisher
- Informa UK Limited
- Published
- 2003-10
- Volume
- 8
- Issue
- 5
- Pages
- 241-245
- ISSN
- 1351-0002 (ISSN-L)
- 1743-2928
- OpenAlex
- W1988041754
- Cited by
- 52
- References
- 15
- Citations by year
- 2025: 2 · 2023: 3 · 2022: 3 · 2021: 2 · 2020: 1 · 2019: 1 · 2018: 4 · 2017: 2 · 2016: 3 · 2015: 3 · 2014: 2 · 2013: 2 · 2012: 2
- FWCI
- 1.12
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Redox Report (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01dk013682-36)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01 DK13682)
- Topics
- Health Sciences › Medicine › Genetics › Hemoglobinopathies and Related Disorders
- Health Sciences › Medicine › Physiology › Erythrocyte Function and Pathophysiology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Hemoglobin structure and function
- Keywords
- beta-thalassemia major, oxidant injury, ineffective erythropoiesis, hemolysis, erythrocyte membrane proteins, band 3, protein 4.1, erythroid precursors
- MeSH terms
- Anion Exchange Protein 1, Erythrocyte, Blood Proteins, Bone Marrow, Cytoskeletal Proteins, Erythropoiesis, Hemolysis, Humans, Lymphoma, Membrane Potentials, Membrane Proteins, Mitochondria, Leukemia, Myelogenous, Chronic, BCR-ABL Positive, Erythroid Precursor Cells, Case-Control Studies, Oxidants, beta-Thalassemia, Apoptosis, Annexin A5, Oxidative Stress, fas Receptor, Caspases, Caspase 8
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