肺纤维化
博莱霉素
肌成纤维细胞
特发性肺纤维化
医学
癌症研究
转化生长因子
纤维化
吡非尼酮
SMAD公司
间质性肺病
信号转导
肺
免疫学
病理
内科学
细胞生物学
生物
化疗
作者
Songtao Gu,Jingjing Liang,Jianwei Zhang,Zhichao Liu,Miao Yang,Yuli Wei,Shimeng Li,Jinying Gu,Yunyao Cui,Ting Xiao,Xiaohe Li,Cheng Yang
出处
期刊:Molecules
[Multidisciplinary Digital Publishing Institute]
日期:2023-02-27
卷期号:28 (5): 2195-2195
被引量:34
标识
DOI:10.3390/molecules28052195
摘要
Idiopathic pulmonary fibrosis (IPF) is a chronic progressive interstitial lung disease with unknown etiology, high mortality and limited treatment options. It is characterized by myofibroblast proliferation and extensive deposition of extracellular matrix (ECM), which will lead to fibrous proliferation and the destruction of lung structure. Transforming growth factor-β1 (TGF-β1) is widely recognized as a central pathway of pulmonary fibrosis, and the suppression of TGF-β1 or the TGF-β1-regulated signaling pathway may thus offer potential antifibrotic therapies. JAK-STAT is a downstream signaling pathway regulated by TGF-β1. JAK1/2 inhibitor baricitinib is a marketed drug for the treatment of rheumatoid arthritis, but its role in pulmonary fibrosis has not been reported. This study explored the potential effect and mechanism of baricitinib on pulmonary fibrosis in vivo and in vitro. The in vivo studies have shown that baricitinib can effectively attenuate bleomycin (BLM)-induced pulmonary fibrosis, and in vitro studies showed that baricitinib attenuates TGF-β1-induced fibroblast activation and epithelial cell injury by inhibiting TGF-β1/non-Smad and TGF-β1/JAK/STAT signaling pathways, respectively. In conclusion, baricitinib, a JAK1/2 inhibitor, impedes myofibroblast activation and epithelial injury via targeting the TGF-β1 signaling pathway and reduces BLM-induced pulmonary fibrosis in mice.
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