Integrating mechanisms of pulmonary fibrosis

被引:1047
作者
Wynn, Thomas A. [1 ,2 ]
机构
[1] NIAID, Program Barrier Immun & Repair, NIH, Bethesda, MD 20892 USA
[2] NIAID, Immunopathogenesis Sect, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA
基金
美国国家卫生研究院;
关键词
TUMOR-NECROSIS-FACTOR; INDUCED LUNG INJURY; BRONCHIOLITIS OBLITERANS SYNDROME; THYMIC STROMAL LYMPHOPOIETIN; MESENCHYMAL STEM-CELLS; GROWTH-FACTOR-BETA; FACTOR-ALPHA; IL-13-INDUCED INFLAMMATION; NALP3; INFLAMMASOME; MURINE LUNG;
D O I
10.1084/jem.20110551
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Pulmonary fibrosis is a highly heterogeneous and lethal pathological process with limited therapeutic options. Although research on the pathogenesis of pulmonary fibrosis has frequently focused on the mechanisms that regulate the proliferation, activation, and differentiation of collagen-secreting myofibroblasts, recent studies have identified new pathogenic mechanisms that are critically involved in the initiation and progression of fibrosis in a variety of settings. A more detailed and integrated understanding of the cellular and molecular mechanisms of pulmonary fibrosis could help pave the way for effective therapeutics for this devastating and complex disease.
引用
收藏
页码:1339 / 1350
页数:12
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