Fujiwara Tohru
Department of Hematology and Rheumatology, Tohoku University Graduate School of Medicine.
Laboratory Diagnostics, Tohoku University Hospital.
Rinsho Ketsueki. 2020;61(7):770-778. doi: 10.11406/rinketsu.61.770.
Ring sideroblasts show abnormal mitochondrial iron accumulation, and their emergence in the bone marrow is a characteristic of sideroblastic anemias (SAs). SAs are a group of heterogeneous congenital and acquired disorders. Congenital SA is a rare disease caused by gene mutations involved in heme biosynthesis, iron-sulfur cluster biosynthesis, and mitochondrial protein synthesis. SAs can also occur after exposure to certain drugs or alcohol and due to copper deficiency (secondary SA). Furthermore, SAs are associated with myelodysplastic syndrome (idiopathic SA), strongly correlating with specific somatic mutations in splicing factor 3b subunit 1 (SF3B1), which is involved in the RNA splicing machinery. Recent reports have indicated that common defects in iron/heme metabolism underlie in the mechanisms of ring sideroblast formation in congenital and acquired SAs. Current understanding of SA pathophysiology, including the mechanisms of ring sideroblast formation, is discussed in this review.
环形铁粒幼细胞表现出线粒体铁异常蓄积,其在骨髓中的出现是铁粒幼细胞性贫血(SA)的一个特征。SA是一组异质性的先天性和获得性疾病。先天性SA是一种罕见疾病,由参与血红素生物合成、铁硫簇生物合成和线粒体蛋白质合成的基因突变引起。SA也可在接触某些药物或酒精后以及由于铜缺乏(继发性SA)而发生。此外,SA与骨髓增生异常综合征(特发性SA)相关,与参与RNA剪接机制的剪接因子3b亚基1(SF3B1)中的特定体细胞突变密切相关。最近的报告表明,先天性和获得性SA中环形铁粒幼细胞形成机制的基础是铁/血红素代谢的常见缺陷。本综述讨论了目前对SA病理生理学的理解,包括环形铁粒幼细胞形成的机制。