期刊
JOURNAL OF CLINICAL INVESTIGATION
卷 119, 期 1, 页码 7-10出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI38084
关键词
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资金
- NHLBI NIH HHS [R37 HL062569, R01 HL064365, HL38621, HL62569, R01 HL038621, R01 HL089445, HL38578, HL64365, R01 HL062569, R01 HL038578, HL89445] Funding Source: Medline
Idiopathic pulmonary fibrosis (IPF) is characterized by progressive (myo)fibroblast accumulation and collagen deposition. One possible source of (myo)fibroblasts is epithelial cells that undergo epithelial-mesenchymal transition (EMT), a process frequently mediated by TGF-beta. In this issue of the JCI, Kim et al. report that epithelial cell-specific deletion of alpha 3 integrin prevents EMT in mice, thereby protecting against bleomycin-induced fibrosis (see the related article beginning on page 213). The authors propose a novel mechanism linking TGF-beta and beta-catenin signaling in EMT through integrin-dependent association of tyrosine-phosphorylated beta-catenin and pSmad2 and suggest targeted disruption of this interaction as a potential therapeutic approach.
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