Research Progress on the Involvement of Aberrant Epigenetic Regulation in the Pathogenesis of Aplastic Anemia
HONG Yaonan1,2, DONG Jingjie1,2, JIA Xinru1,2, WANG Peicheng2, YANG Xiawan1,2,3, SHEN Yingying1,2,3, WU Dijiong1,2,3*
AA (aplastic anemia) is a bone marrow failure disorder characterized by impaired hematopoietic function, with its pathogenesis not yet fully elucidated. Historically, its complex etiology has been primarily attrib uted to hematopoietic stem cell damage resulting from immune system dysregulation. In recent years, an increas ing number of studies have observed aberrant epigenetic modifications in AA patients, which participate in disease pathogenesis by influencing the expression and regulation of hematopoiesis-associated genes. These alterations particularly involve genes related to autoimmune responses and bone marrow failure, offering insights into prognosis and clinical outcomes. Specific epigenetic changes have demonstrated potential as biomarkers for assessing disease status, therapeutic response, and prognosis prediction in AA. Owing to the pathogenic features and reversible nature of epigenetic modifications, therapies targeting epigenetic mechanisms (such as enhancing hematopoietic stem cell expansion and modulating the immune microenvironment) provide novel perspectives for advancing AA treatment. This review outlines current research progress on aberrant epigenetic regulation in AA pathogenesis, encompassing DNA methylation, histone modifications, and non-coding RNA-mediated regulation based on recent studies.
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