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10.1186/s12931-020-01445-6

http://scihub22266oqcxt.onion/10.1186/s12931-020-01445-6
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32664949!7359430!32664949
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suck abstract from ncbi


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pmid32664949      Respir+Res 2020 ; 21 (1): 182
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  • SARS-CoV-2 induces transcriptional signatures in human lung epithelial cells that promote lung fibrosis #MMPMID32664949
  • Xu J; Xu X; Jiang L; Dua K; Hansbro PM; Liu G
  • Respir Res 2020[Jul]; 21 (1): 182 PMID32664949show ga
  • BACKGROUND: Severe acute respiratory syndrome (SARS)-CoV-2-induced coronavirus disease-2019 (COVID-19) is a pandemic disease that affects > 2.8 million people worldwide, with numbers increasing dramatically daily. However, there is no specific treatment for COVID-19 and much remains unknown about this disease. Angiotensin-converting enzyme (ACE)2 is a cellular receptor of SARS-CoV-2. It is cleaved by type II transmembrane serine protease (TMPRSS)2 and disintegrin and metallopeptidase domain (ADAM)17 to assist viral entry into host cells. Clinically, SARS-CoV-2 infection may result in acute lung injury and lung fibrosis, but the underlying mechanisms of COVID-19 induced lung fibrosis are not fully understood. METHODS: The networks of ACE2 and its interacting molecules were identified using bioinformatic methods. Their gene and protein expressions were measured in human epithelial cells after 24 h SARS-CoV-2 infection, or in existing datasets of lung fibrosis patients. RESULTS: We confirmed the binding of SARS-CoV-2 and ACE2 by bioinformatic analysis. TMPRSS2, ADAM17, tissue inhibitor of metalloproteinase (TIMP)3, angiotensinogen (AGT), transformation growth factor beta (TGFB1), connective tissue growth factor (CTGF), vascular endothelial growth factor (VEGF) A and fibronectin (FN) were interacted with ACE2, and the mRNA and protein of these molecules were expressed in lung epithelial cells. SARS-CoV-2 infection increased ACE2, TGFB1, CTGF and FN1 mRNA that were drivers of lung fibrosis. These changes were also found in lung tissues from lung fibrosis patients. CONCLUSIONS: Therefore, SARS-CoV-2 binds with ACE2 and activates fibrosis-related genes and processes to induce lung fibrosis.
  • |*Gene Expression Regulation[MESH]
  • |Angiotensin-Converting Enzyme 2[MESH]
  • |COVID-19[MESH]
  • |China[MESH]
  • |Coronavirus Infections/epidemiology/*genetics/physiopathology[MESH]
  • |Disease Progression[MESH]
  • |Epithelial Cells/cytology/metabolism[MESH]
  • |Female[MESH]
  • |Humans[MESH]
  • |Male[MESH]
  • |Pandemics/statistics & numerical data[MESH]
  • |Peptidyl-Dipeptidase A/*genetics[MESH]
  • |Pneumonia, Viral/epidemiology/*genetics/physiopathology[MESH]
  • |Prevalence[MESH]
  • |Pulmonary Fibrosis/epidemiology/etiology/*genetics[MESH]
  • |Receptors, Virus/metabolism[MESH]
  • |Respiratory Distress Syndrome/diagnosis/epidemiology/*genetics[MESH]
  • |Risk Assessment[MESH]
  • |Severe acute respiratory syndrome-related coronavirus/*genetics[MESH]
  • |Survival Analysis[MESH]
  • |Transcription, Genetic[MESH]


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