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10.1007/s10517-017-3678-1

http://scihub22266oqcxt.onion/10.1007/s10517-017-3678-1
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28361411!ä!28361411

suck abstract from ncbi


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pmid28361411      Bull+Exp+Biol+Med 2017 ; 162 (5): 647-649
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  • Study of SMAD-Dependent Signal Pathway in the Development of Early Pulmonary Fibrosis in Mice Infected with Influenza A/H1N1 Virus #MMPMID28361411
  • Shatskaya EV; Kovner AV; Potapova OV; Cherdantseva LA; Shkurupy VA; Shestopalov AM
  • Bull Exp Biol Med 2017[Mar]; 162 (5): 647-649 PMID28361411show ga
  • Early fibrosis of the visceral organs is one of the main complications of infection caused by influenza A virus. Structural manifestations and molecular regulators of the epithelialmesenchymal transformation as a possible mechanism of fibrosis progression were studied in mice infected with influenza A/H1N1 A/Tomsk/13/2010 virus. We found early fibrosis of the lungs against the background of minor changes in fibroblast count. However, enhanced expression of TGF-beta and SMAD-2 by macrophages and alveolocytes attested to possible development of epithelial-mesenchymal transformation and its contribution to activation of fibrogenesis process in the lungs.
  • |Animals[MESH]
  • |Animals, Outbred Strains[MESH]
  • |Humans[MESH]
  • |Influenza A Virus, H1N1 Subtype[MESH]
  • |Influenza, Human/*metabolism/virology[MESH]
  • |Lung/pathology/virology[MESH]
  • |Male[MESH]
  • |Mice[MESH]
  • |Pulmonary Fibrosis/*metabolism/virology[MESH]
  • |Signal Transduction[MESH]


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