嘌呤能途径及其在治疗急性髓性白血病中的临床应用。

IF 2.4 4区 医学 Q2 NEUROSCIENCES
Purinergic Signalling Pub Date : 2025-08-01 Epub Date: 2024-03-06 DOI:10.1007/s11302-024-09997-8
Huijuan Wang, Yujie Wei, Na Wang
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引用次数: 0

摘要

尽管使用了造血干细胞移植和嵌合抗原受体T细胞疗法(CAR-T)等多种疗法,急性髓性白血病(AML)患者的预后仍然普遍较差。然而,免疫疗法是目前治疗血液肿瘤的热门话题。细胞外三磷酸腺苷(ATP)可通过 CD39 转化为二磷酸腺苷(ADP),ADP 可通过 CD73 转化为腺苷,腺苷可与 P1 和 P2 受体结合,从而发挥免疫调节作用。对嘌呤能信号通路机制的研究可为急性髓细胞白血病的治疗提供新的方向,目前已有一些研究人员发现了该信号通路的抑制剂,并逐步应用于临床。本文阐述了嘌呤能信号通路的机制及其临床应用,揭示了治疗急性髓细胞性白血病的新靶点,进而改善患者预后。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Purinergic pathways and their clinical use in the treatment of acute myeloid leukemia.

Despite the use of various therapies such as hematopoietic stem cell transplantation and chimeric antigen receptor T cell therapy (CAR-T), the prognosis of patients with acute myeloid leukemia (AML) is still generally poor. However, immunotherapy is currently a hot topic in the treatment of hematological tumors. Extracellular adenosine triphosphate (ATP) can be converted to adenosine diphosphate (ADP) via CD39, and ADP can be converted to adenosine via CD73, which can bind to P1 and P2 receptors to exert immunomodulatory effects. Research on the mechanism of the purinergic signaling pathway can provide a new direction for the treatment of AML, and inhibitors of this signaling pathway have been discovered by several researchers and gradually applied in the clinic. In this paper, the mechanism of the purinergic signaling pathway and its clinical application are described, revealing a new target for the treatment of AML and subsequent improvement in patient prognosis.

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来源期刊
Purinergic Signalling
Purinergic Signalling 医学-神经科学
CiteScore
6.60
自引率
17.10%
发文量
75
审稿时长
6-12 weeks
期刊介绍: Nucleotides and nucleosides are primitive biological molecules that were utilized early in evolution both as intracellular energy sources and as extracellular signalling molecules. ATP was first identified as a neurotransmitter and later as a co-transmitter with all the established neurotransmitters in both peripheral and central nervous systems. Four subtypes of P1 (adenosine) receptors, 7 subtypes of P2X ion channel receptors and 8 subtypes of P2Y G protein-coupled receptors have currently been identified. Since P2 receptors were first cloned in the early 1990’s, there is clear evidence for the widespread distribution of both P1 and P2 receptor subtypes in neuronal and non-neuronal cells, including glial, immune, bone, muscle, endothelial, epithelial and endocrine cells.
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