综述白细胞介素6与肺纤维化*
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滨州医学院附属医院

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R563.9

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国家自然科学基金面上项目(No. 82172565) [通讯作者]:邓炯,E-mail: jiongdeng@bzmc.edu.cn;Tel: 0543-3258042,国家自然科学基金项目(面上项目,重点项目,重大项目)


Interleukin-6 and lung fibroblast*
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    摘要:

    特发性肺纤维化(IPF)是一种进行性晚期肺部疾病,目前尚无治愈方法。IPF的主要特征是肺上皮细胞受损,活化的肺成纤维细胞和肌成纤维细胞过度沉积细胞外基质(ECM)蛋白,导致气体交换减少和肺功能受损。白细胞介素6(IL-6)由免疫细胞对组织损伤迅速反应产生,对细胞过程如急性反应、造血和免疫反应具有广泛的影响。此外,在以纤维化为特征的各种慢性炎症性疾病中发现了高水平的IL-6,并且该因子通过Janus激酶/信号转导子和转录激活蛋白3(JAK/STAT3)的激活在各种器官的纤维化中发挥重要作用。在这里,我们回顾了IL-6在肺纤维化中的作用,为开发减轻肺纤维化疾病发展和促进肺纤维化损伤解决的疗法提供了机会。

    Abstract:

    Idiopathic pulmonary fibrosis (IPF) is a progressive and advanced lung disease for which there is no effective treatment at present. The main features of IPF include the damage to the lung epithelial cells along with the excessive depositing extracellular matrix (ECM) secreted from the activated lung fibroblasts and myofibroblasts, whereby leading to reduced air exchange and then impaired lung function. Interleukin-6 (IL-6), which is produced from immune cells, is rapid for response to the tissue injury and has a broad impact on cellular processes such as acute reactions, hematopoiesis, and immune responses. Additionally, elevated levels of IL-6 have been found in various chronic inflammatory diseases characterized by fibrosis and IL-6 plays an important role via activation of Janus kinases/signal transducers and activators of transcription 3 (JAK/STAT3) signaling in the fibrosis of any organ system. Here, we explore the role of IL-6 in pulmonary fibrosis and then providing a therapeutic approach for alleviating the development of pulmonary fibrosis disease and improving the resolution of pulmonary fibrosis damage.

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  • 收稿日期:2023-05-25
  • 最后修改日期:2023-08-04
  • 录用日期:2023-09-05
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