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    <title>DSpace Собрание: American Journal of Respiratory Cell and Molecular Biology Publishes the most significant and original observations in the area of respiratory and lung cell biology</title>
    <link>http://hdl.handle.net/20.500.12701/1705</link>
    <description>American Journal of Respiratory Cell and Molecular Biology Publishes the most significant and original observations in the area of respiratory and lung cell biology</description>
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    <dc:date>2024-02-19T01:15:58Z</dc:date>
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    <title>Sustained Smad2 Phosphorylation Is Required for Myofibroblast Transformation in Response to TGF-β</title>
    <link>http://hdl.handle.net/20.500.12701/1706</link>
    <description>Название: Sustained Smad2 Phosphorylation Is Required for Myofibroblast Transformation in Response to TGF-β
Авторы: Ard, Shawn; Reed, Eleanor B.; Smolyaninova, Larisa V.; Orlov, Sergei N.; Mutlu, Gökhan M.; Guzy, Robert D.; Dulin, Nickolai O.
Краткий осмотр (реферат): Idiopathic pulmonary fibrosis (IPF) is a progressive, fatal disease characterized by parenchymal fibrosis and structural distortion of the lungs. IPF is believed to be a disorder of abnormal wound healing, wherein the initial trigger to the fibrotic response is injury to the alveolar epithelial cells, followed by an exuberant, nonresolving wound-healing response (1). Injury of alveolar epithelial cells results in the elaboration of a fibrinous matrix and activation of several profibrotic mediators, of which transforming growth factor β (TGF-β) is the most established. Lung-targeted overexpression of TGF-β results in the development of lung fibrosis in animals. Conversely, inhibition of TGF-β can inhibit in vivo fibrogenesis...</description>
    <dc:date>2019-03-01T00:00:00Z</dc:date>
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