Signaling pathways in the epithelial origins of pulmonary fibrosis

被引:84
作者
Hardie, William D. [1 ,3 ]
Hagood, James S. [1 ]
Dave, Vrushank [2 ]
Perl, Anne-Karina T. [2 ]
Whitsett, Jeffrey A. [2 ]
Korfhagen, Thomas R. [2 ]
Glasser, Stephan [2 ]
机构
[1] Univ Calif San Diego, Dept Pediat, San Diego, CA 92103 USA
[2] Univ Calif San Diego, Dept Pulm Biol, Cincinnati Childrens Med Ctr, San Diego, CA 92103 USA
[3] Univ Calif San Diego, Dept Pulm Med, San Diego, CA 92103 USA
基金
美国国家卫生研究院;
关键词
epithelial mesenchymal transition; epidermal growth factor receptor; transforming growth factor alpha; EPIDERMAL-GROWTH-FACTOR; FACTOR-ALPHA; MESENCHYMAL TRANSITION; FACTOR-RECEPTOR; CIRCULATING FIBROCYTES; LUNG-DISEASE; GENE-EXPRESSION; STEM-CELLS; ACTIVATION; RAPAMYCIN;
D O I
10.4161/cc.9.14.12268
中图分类号
Q2 [细胞生物学];
学科分类号
071013 [干细胞生物学];
摘要
Pulmonary fibrosis complicates a number of disease processes and leads to substantial morbidity and mortality. Idiopathic pulmonary fibrosis (IPF) is perhaps the most pernicious and enigmatic form of the greater problem of lung fibrogenesis with a median survival of three years from diagnosis in affected patients. In this review, we will focus on the pathology of IPF as a model of pulmonary fibrotic processes, review possible cellular mechanisms, review current treatment approaches and review two transgenic mouse models of lung fibrosis to provide insight into processes that cause lung fibrosis. We will also summarize the potential utility of signaling pathway inhibitors as a future treatment in pulmonary fibrosis. Finally, we will present data demonstrating a minimal contribution of epithelial-mesenchymal transition in the development of fibrotic lesions in the transforming growth factor-alpha transgenic model of lung fibrosis.
引用
收藏
页码:2769 / 2776
页数:8
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