【摘要】 人口老龄化是当今全球面临的重要挑战，其中炎性老化作为衰老的核心特征之一，与多种老年疾病的发生发展密切相关。造血干细胞（hematopoietic stem cell,HSC）的髓系分化偏倚是免疫衰老的关键表现，表现为HSC向髓系细胞分化增加而向淋巴系分化减少，导致免疫功能失调并驱动慢性炎症。文章系统阐述HSC髓系分化偏倚与炎性老化的相互作用机制，包括骨髓微环境炎症、表观遗传改变以及线粒体功能障碍。此外，总结靶向干预策略，如阻断白细胞介素1信号通路、调控表观遗传修饰、重塑骨髓微环境及清除衰老细胞，这些措施在动物模型中显示出逆转髓系分化偏倚和改善免疫功能的潜力。更多还原

【Abstract】 Population aging is a major global challenge today,in which inflammaging,as one of the core features of aging,is closely associated with the development of various age-related diseases. Myeloid-biased differentiation of hematopoietic stem cell(HSC)is a key manifestation of immunosenescence,characterized by enhanced differentiation of HSC into myeloid cells and reduced lymphoid differentiation,leading to immune dysfunction and driving chronic inflammation. This review systematically elucidates the interaction mechanisms between HSC myeloid-biased differentiation and inflammaging,including bone marrow microenvironment inflammation,epigenetic alterations,and mitochondrial dysfunction. Furthermore,it summarizes targeted intervention strategies,such as blocking the interleukin-1 signaling pathway,modulating epigenetic modifications,remodeling the bone marrow microenvironment,and clearing senescent cells,which have shown potential in animal models to reverse myeloid-biased differentiation and improve immune function.更多还原