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中国防痨杂志 ›› 2024, Vol. 46 ›› Issue (8): 971-975.doi: 10.19982/j.issn.1000-6621.20240103

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基于核因子κB受体活化因子配体信号通路激活破骨细胞治疗骨结核的研究进展

田宏晶1, 张彦军2, 邓强2(), 李军杰2, 杨军1, 刘鑫锋1, 杜建强1   

  1. 1甘肃中医药大学研究生院,兰州 730030
    2甘肃省中医院,兰州 730050
  • 收稿日期:2024-03-20 出版日期:2024-08-10 发布日期:2024-08-01
  • 通信作者: 邓强 E-mail:dengqiang11576@sohu.com
  • 基金资助:
    2021年甘肃省财政转移支付地方项目(20210140305);2022年甘肃省科技计划项目(22JR5RA624);2023年甘肃省卫生健康行业项目(GSWSKY2023-27)

Research progress on osteoclasts activated by receptor activator of nuclear factor-κB ligand signaling pathway for the treatment of bone tuberculosis

Tian Hongjing1, Zhang Yanjun2, Deng Qiang2(), Li Junjie2, Yang Jun1, Liu Xinfeng1, Du Jianqiang1   

  1. 1Graduate School of Gansu University of Chinese Medicine,Lanzhou 730030, China
    2Gansu Provincial Hospital of Traditional Chinese Medicine, Lanzhou 730050, China
  • Received:2024-03-20 Online:2024-08-10 Published:2024-08-01
  • Contact: Deng Qiang E-mail:dengqiang11576@sohu.com
  • Supported by:
    Fiscal Transfer Payment Local Project of Gansu Province in 2021(20210140305);Science and Technology Plan Projects in Gansu Province in 2022(22JR5RA624);Health Industry Project of Gansu Province in 2023(GSWSKY2023-27)

摘要:

骨结核是一种严重危害人体健康的骨科感染性疾病,其病灶组织破坏的最大特点是骨质的吸收及破坏,其中破骨细胞是骨吸收的主要细胞。破骨细胞是由造血干细胞分化而来的多核细胞,通常是由核因子κB受体活化因子配体(receptor activator of nuclear factor-κB ligand,RANKL)与核因子κB受体活化因子(receptor activator for nuclear factor-κB,RANK)调控产生。结核分枝杆菌可以通过RANKL信号通路激活破骨细胞生成转录因子,以增强破骨细胞对骨质的吸收。笔者通过综述RANKL信号通路的结构及破骨细胞的研究进展,以及它们在骨结核临床治疗中可能发挥的潜在作用,为该领域的研究提供新的思路。

关键词: 结核,骨关节, 核因子κB受体活化因子, 信号传导, 破骨细胞, 总结性报告(主题)

Abstract:

Bone tuberculosis represents a grave orthopedic infectious disease that poses significant threats to human health. The hallmark of the disease is the absorption and subsequent destruction of bone tissue, primarily mediated by osteoclasts. These multinucleated cells, originating from hematopoietic stem cells, are primarily regulated by the receptor activator of nuclear factor-κB ligand (RANKL) and its receptor, RANK. Mycobacterium tuberculosis triggers osteoclasts to produce transcription factors via the RANKL signaling pathway, thus intensifying the degradation of bone. This review delineates the architecture of the RANKL signaling pathway, explores recent advances in osteoclast research, and discusses their prospective applications in the clinical management of bone tuberculosis, offering novel insights for future investigations.

Key words: Tuberculosis, osteoarticular, Receptor activator of nuclear factor-kappa B, Signal transduction, Osteoclasts, Summary report

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