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10.1016/j.autrev.2020.102571

http://scihub22266oqcxt.onion/10.1016/j.autrev.2020.102571
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suck abstract from ncbi


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pmid32376402      Autoimmun+Rev 2020 ; 19 (7): 102571
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  • Transcriptional landscape of SARS-CoV-2 infection dismantles pathogenic pathways activated by the virus, proposes unique sex-specific differences and predicts tailored therapeutic strategies #MMPMID32376402
  • Fagone P; Ciurleo R; Lombardo SD; Iacobello C; Palermo CI; Shoenfeld Y; Bendtzen K; Bramanti P; Nicoletti F
  • Autoimmun Rev 2020[Jul]; 19 (7): 102571 PMID32376402show ga
  • The emergence of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) disease (COVID-19) has posed a serious threat to global health. As no specific therapeutics are yet available to control disease evolution, more in-depth understanding of the pathogenic mechanisms induced by SARS-CoV-2 will help to characterize new targets for the management of COVID-19. The present study identified a specific set of biological pathways altered in primary human lung epithelium upon SARS-CoV-2 infection, and a comparison with SARS-CoV from the 2003 pandemic was studied. The transcriptomic profiles were also exploited as possible novel therapeutic targets, and anti-signature perturbation analysis predicted potential drugs to control disease progression. Among them, Mitogen-activated protein kinase kinase (MEK), serine-threonine kinase (AKT), mammalian target of rapamycin (mTOR) and I kappa B Kinase (IKK) inhibitors emerged as candidate drugs. Finally, sex-specific differences that may underlie the higher COVID-19 mortality in men are proposed.
  • |*Sex Factors[MESH]
  • |Betacoronavirus[MESH]
  • |COVID-19[MESH]
  • |Cells, Cultured[MESH]
  • |Coronavirus Infections/*genetics/*mortality/pathology[MESH]
  • |Drug Discovery[MESH]
  • |Epithelial Cells/virology[MESH]
  • |Female[MESH]
  • |Humans[MESH]
  • |Lung/cytology[MESH]
  • |Male[MESH]
  • |Pandemics[MESH]
  • |Pneumonia, Viral/*genetics/*mortality/pathology[MESH]
  • |SARS-CoV-2[MESH]
  • |Severe Acute Respiratory Syndrome[MESH]
  • |TOR Serine-Threonine Kinases[MESH]


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