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。
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.
作者
盛琪
童瑾
SHENG Qi;TONG Jin(Department of Respiratory and Critical Care Medicine,the Second Affiliated Hospital of Chongqing Medical University,Chongqing 400010,China)
出处
《基础医学与临床》
CAS
2024年第6期892-896,共5页
Basic and Clinical Medicine
基金
重庆市卫生适宜技术推广项目(2022jstg021)。
