In eukaryotic RNA, N6‐methyladenosine (m6A) is a prevalent form of methylation modification. The m6A modification process is reversible and dynamic, written by m6A methyltransferase complex, erased by m6A demethylase, and recognized by m6A binding proteins. Through mediating RNA stability, decay, alternative splicing, and translation processes, m6A modification regulates gene expression at the post‐transcriptional level. Erythropoiesis is the process of hematopoietic stem cells undergoing proliferation, a series of differentiation and maturation to form red blood cells (RBCs). Thalassemia is a common monogenic disease characterized by excessive production of ineffective RBCs in the peripheral circulation, resulting in hemolytic anemia. Increasing evidence suggests that m6A modification plays a crucial role in erythropoiesis. In this review, we comprehensively summarize the function of m6A modification in erythropoiesis and further generalize the mechanism of m6A modification regulating ineffective erythropoiesis and fetal hemoglobin expression. The purpose is to improve the understanding of the pathogenesis of erythroid dysplasia and offer new perspectives for the diagnosis and treatment of thalassemia.

中文翻译：

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N6-甲基腺苷修饰在红细胞生成和地中海贫血中的调节

在真核生物RNA中，N6‐甲基腺苷（m6A) 是甲基化修饰的一种普遍形式。他们6一个修改过程是可逆的、动态的，由 m 编写6甲基转移酶复合物，被 m 擦除6一种去甲基化酶，并被 m 识别6一种结合蛋白。通过介导 RNA 稳定性、衰变、选择性剪接和翻译过程，m6修饰在转录后水平调节基因表达。红细胞生成是造血干细胞经历增殖、一系列分化和成熟形成红细胞（RBC）的过程。地中海贫血是一种常见的单基因疾病，其特征是外周循环中无效红细胞过多产生，导致溶血性贫血。越来越多的证据表明，m6修饰在红细胞生成中起着至关重要的作用。在这篇综述中，我们全面总结了m的功能6红细胞生成的改变并进一步概括 m 的机制6调节无效红细胞生成和胎儿血红蛋白表达的修饰。目的是提高对红系发育不良发病机制的认识，为地中海贫血的诊断和治疗提供新的视角。