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• W2019305952 endingPage "133" @default.
• W2019305952 startingPage "120" @default.
• W2019305952 abstract "Sideroblastic anemias are a heterogeneous group of disorders, characterized by mitochondrial iron overload in developing red blood cells. The unifying characteristic of all sideroblastic anemias is the ring sideroblast, which is a pathological erythroid precursor containing excessive deposits of non-heme iron in mitochondria with perinuclear distribution creating a ring appearance. Sideroblastic anemias may be hereditary or acquired. Hereditary sideroblastic anemias are caused by defects in genes present on the X chromosome (mutations in the <i>ALAS2</i>, <i>ABCB7</i>, or <i>GRLX5</i> gene), genes on autosomal chromosomes, or mitochondrial genes. Acquired sideroblastic anemias are either primary (refractory anemia with ring sideroblasts, RARS, representing one subtype of the myelodysplastic syndrome) or secondary due to some drugs, toxins, copper deficiency, or chronic neoplastic disease. The pathogenesis of mitochondrial iron loading in developing erythroblasts is diverse. Ring sideroblasts can develop as a result of a heme synthesis defect in erythroblasts (ALAS2 mutations), a defect in iron-sulfur cluster assembly, iron-sulfur protein precursor release from mitochondria (ABCB7 mutations), or by a defect in intracellular iron metabolism in erythroid cells (e.g. RARS)." @default.
• W2019305952 created "2016-06-24" @default.
• W2019305952 creator A5042381475 @default.
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• W2019305952 date "2009-01-01" @default.
• W2019305952 modified "2023-10-03" @default.
• W2019305952 title "Mitochondrial Iron Metabolism and Sideroblastic Anemia" @default.
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• W2019305952 doi "https://doi.org/10.1159/000243796" @default.
• W2019305952 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19907149" @default.
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