基础医学与临床 ›› 2024, Vol. 44 ›› Issue (6): 892-896.doi: 10.16352/j.issn.1001-6325.2024.06.0892

• 短篇综述 • 上一篇    下一篇

CXCL10/CXCR3轴在急性呼吸窘迫综合征中的作用

盛琪, 童瑾*   

  1. 重庆医科大学附属第二医院 呼吸与危重症医学科,重庆 400010
  • 收稿日期:2023-09-15 修回日期:2023-12-27 出版日期:2024-06-05 发布日期:2024-05-24
  • 通讯作者: *tongjin01234@163.com
  • 基金资助:
    重庆市卫生适宜技术推广项目(2022jstg021)

The CXCL10/CXCR3 axis in acute respiratory distress syndrome

SHENG Qi, TONG Jin*   

  1. Department of Respiratory and Critical Care Medicine, the Second Affiliated Hospital of Chongqing Medical University,Chongqing 400010,China
  • Received:2023-09-15 Revised:2023-12-27 Online:2024-06-05 Published:2024-05-24
  • Contact: *tongjin01234@163.com

摘要: CXC趋化因子配体10(CXCL10)/ CXC趋化因子受体3(CXCR3)信号轴是介导Th1型免疫反应的重要通路,通过放大炎性风暴广泛参与急性呼吸窘迫综合征(ARDS)的发生发展,同时促进血管内皮凋亡、抑制修复可增加肺血管血栓形成的可能,此外也因可调节细胞迁移、限制细胞外基质沉积发挥抗肺纤维化的保护作用。本文系统讨论了CXCL10/CXCR3信号轴在ARDS发生发展作用中的不同调节机制,为ARDS的诊治提供新思考和潜在可能性。

关键词: CXCL10/CXCR3, 急性呼吸窘迫综合征, 炎性反应, 肺血管栓塞, 肺纤维化

Abstract: The CXC chemokine ligand-10/CXC receptor-3 (CXCL10/CXCR3) axis, a crucial pathway mediating Th1-type immunity, substantially contributes to the development of acute respiratory distress syndrome(ARDS) by enhancing inflammatory storms. It additionally promotes vascular endothelial apoptosis and impedes vasculature repair, elevating the risk of pulmonary vascular thrombosis. Conversely, this axis plays a protective role in limiting extra-cellular matrix deposition and modulating cell migration, thereby mitigating pulmonary fibrosis. The various mechanisms of the CXCL10/CXCR3 axis in the pathogenesis and progression of ARDS could offer novel insights for the diagnosis and treatment of ARDS.

Key words: CXCL10/CXCR3 axis, acute respiratory distress syndrome, inflammations, pulmonary embolism, pulmonary fibrosis

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