肺纤维化
特发性肺纤维化
肺
生物
纤维化
上皮-间质转换
信号转导
癌症研究
病理
疾病
免疫学
生物信息学
医学
内科学
细胞生物学
下调和上调
癌症
遗传学
转移
基因
生物化学
作者
William D. Hardie,James S. Hagood,Vrushank Davé,Anne‐Karina T. Perl,Anne‐Karina T. Perl,Jeffrey A. Whitsett,Thomas R. Korfhagen,Stephan W. Glasser
出处
期刊:Cell Cycle
[Informa]
日期:2010-07-15
卷期号:9 (14): 2841-2848
被引量:67
标识
DOI:10.4161/cc.9.14.12268
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.
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