详细信息
骨髓微环境转换与急性髓系白血病化疗耐药相关性的研究进展
Research progress on the correlation between bone marrow microenvironment remodeling and chemotherapy resistance in acute myeloid leukemia
文献类型:期刊文献
中文题名:骨髓微环境转换与急性髓系白血病化疗耐药相关性的研究进展
英文题名:Research progress on the correlation between bone marrow microenvironment remodeling and chemotherapy resistance in acute myeloid leukemia
作者:曲浩铭(综述)[1];李海鹰(审校)[1]
第一作者:曲浩铭
机构:[1]甘肃中医药大学公共卫生学院,甘肃兰州730000
第一机构:甘肃中医药大学公共卫生学院
年份:2026
卷号:39
期号:2
起止页码:237
中文期刊名:中国生物制品学杂志
外文期刊名:Chinese Journal of Biologicals
基金:甘肃省青年博士基金(2021QB-081);2024甘肃省级科技计划(24JRRA1050);2021甘肃省高等学校创新基金(2021A-086)。
语种:中文
中文关键词:急性髓系白血病;骨髓微环境;炎性微环境;免疫微环境;代谢重编程
外文关键词:Acute myeloid leukemia(AML);Bone marrow microenvironment(BMM);Inflammatory microenvironment;Immune microenvironment;Metabolic reprogramming
摘要:作为具有高度侵袭性与复发倾向的恶性肿瘤,急性髓系白血病(acute myeloid leukemia,AML)的发病与骨髓微环境(bone marrow microenvironment,BMM)的恶性转换密切相关。AML细胞通过与BMM的相互作用,促进了炎性、免疫以及代谢微环境的转换,导致正常的造血微环境转变为有利于AML细胞生存和发展的恶性BMM。而重塑后的BMM又促使AML细胞获得耐药性,从而形成一个恶性动态循环。打破这一循环的关键在于:(1)靶向炎性因子[如白细胞介素-6(interleukin-6,IL-6)/JAK/STAT通路];(2)抑制免疫检查点分子[如程序性死亡配体-1(programmed death ligand-1,PD-L1)]或免疫抑制细胞;(3)阻断代谢重编程(如有氧糖酵解、线粒体转移)。基于此,本文对AML发生发展过程中,BMM在相关层面的双向调控作用作一综述,以期在靶向BMM转换机制的治疗策略以及AML耐药的干预措施方面,发现新的思路和潜在的研究治疗靶点。
As a malignant tumor with high invasiveness and a tendency to recur,the pathogenesis of acute myeloid leukemia(AML)is closely related to the malignant transformation of the bone marrow microenvironment(BMM).AML cells promote the transformation of inflammatory,immune,and metabolic microenvironments through their interaction with the BMM,resulting in the normal hematopoietic microenvironment being converted into a malignant one that favors the survival and development of AML cells.The restructured BMM,in turn,facilitates the acquisition of drug resistance by AML cells,thus forming a malignant dynamic cycle.The key to breaking this cycle lies in:(1)targeting inflammatory factors[such as the interleukin-6(IL-6)/JAK/STAT pathway];(2)inhibiting immune checkpoint molecules[such as programmed death ligand-1(PD-L1)]or immune suppressive cells;(3)blocking metabolic reprogramming(such as aerobic glycolysis,mitochondrial transfer).Based on this,this paper reviews the bidirectional regulatory role of the BMM at relevant levels during the development of AML,with the aim of discovering new ideas and potential research targets in therapeutic strategies targeting the transformation mechanisms of the BMM and interventions for AML resistance.
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