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10.1038/s41392-020-00334-0 http://scihub22266oqcxt.onion/10.1038/s41392-020-00334-0 33037188!7545816!33037188     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Signal+Transduct+Target+Ther 2020 ; 5 (1): 235 Nephropedia Template TP {{tp|p=33037188|t=2020. SARS-CoV-2 triggers inflammatory responses and cell death through caspase-8 activation |pdf=|usr=}}{{33037188}} gab.com Text SARS-CoV-2 triggers inflammatory responses and cell death through caspase-8 activation JO: Signal Transduct Target Ther http://www.kidney.de/pget.php?&tw=1&pmid=33037188 #FOAvip Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection can lead to respiratory illness and multi-organ failure in critically ill patients. Although the virus-induced lung damage and inflammatory cytokine storm are believed to be directly associated with coronavirus disease 2019 (COVID-19) clinical manifestations, the underlying mechanisms of virus-triggered inflammatory responses are currently unknown. Here we report that SARS-CoV-2 infection activates caspase-8 to trigger cell apoptosis and inflammatory cytokine processing in the lung epithelial cells. The processed inflammatory cytokines are released through the virus-induced necroptosis pathway. Virus-induced apoptosis, necroptosis, and inflammation activation were also observed in the lung sections of SARS-CoV-2-infected HFH4-hACE2 transgenic mouse model, a valid model for studying SARS-CoV-2 pathogenesis. Furthermore, analysis of the postmortem lung sections of fatal COVID-19 patients revealed not only apoptosis and necroptosis but also massive inflammatory cell infiltration, necrotic cell debris, and pulmonary interstitial fibrosis, typical of immune pathogenesis in the lung. The SARS-CoV-2 infection triggered a dual mode of cell death pathways and caspase-8-dependent inflammatory responses may lead to the lung damage in the COVID-19 patients. These discoveries might assist the development of therapeutic strategies to treat COVID-19. Twit Text FOAVip SARS-CoV-2 triggers inflammatory responses and cell death through caspase-8 activation ????Signal Transduct Target Ther http://www.kidney.de/pget.php?&tw=1&pmid=33037188 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33037188 #FOAvip English Wikipedia <ref>{{Cite pmid|33037188}}</ref> SARS-CoV-2 triggers inflammatory responses and cell death through caspase-8 activation #MMPMID33037188 Li S; Zhang Y; Guan Z; Li H; Ye M; Chen X; Shen J; Zhou Y; Shi ZL; Zhou P; Peng K Signal Transduct Target Ther 2020[Oct]; 5 (1): 235 PMID33037188show ga Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection can lead to respiratory illness and multi-organ failure in critically ill patients. Although the virus-induced lung damage and inflammatory cytokine storm are believed to be directly associated with coronavirus disease 2019 (COVID-19) clinical manifestations, the underlying mechanisms of virus-triggered inflammatory responses are currently unknown. Here we report that SARS-CoV-2 infection activates caspase-8 to trigger cell apoptosis and inflammatory cytokine processing in the lung epithelial cells. The processed inflammatory cytokines are released through the virus-induced necroptosis pathway. Virus-induced apoptosis, necroptosis, and inflammation activation were also observed in the lung sections of SARS-CoV-2-infected HFH4-hACE2 transgenic mouse model, a valid model for studying SARS-CoV-2 pathogenesis. Furthermore, analysis of the postmortem lung sections of fatal COVID-19 patients revealed not only apoptosis and necroptosis but also massive inflammatory cell infiltration, necrotic cell debris, and pulmonary interstitial fibrosis, typical of immune pathogenesis in the lung. The SARS-CoV-2 infection triggered a dual mode of cell death pathways and caspase-8-dependent inflammatory responses may lead to the lung damage in the COVID-19 patients. These discoveries might assist the development of therapeutic strategies to treat COVID-19. |Animals[MESH] |Apoptosis/*immunology[MESH] |Betacoronavirus/*pathogenicity[MESH] |COVID-19[MESH] |Caspase 8/genetics/*immunology[MESH] |Cell Line, Tumor[MESH] |Chemokine CCL5/genetics/immunology[MESH] |Chemokine CXCL10/genetics/immunology[MESH] |Coronavirus Infections/genetics/*immunology/pathology/virology[MESH] |Cytokine Release Syndrome/genetics/*immunology/pathology/virology[MESH] |Disease Models, Animal[MESH] |Epithelial Cells/immunology/pathology/virology[MESH] |Gene Expression Regulation[MESH] |Humans[MESH] |Interleukin-1beta/genetics/immunology[MESH] |Interleukin-7/genetics/immunology[MESH] |Interleukin-8/genetics/immunology[MESH] |Lung/immunology/pathology/virology[MESH] |Mice[MESH] |Mice, Transgenic[MESH] |Necroptosis/*immunology[MESH] |Pandemics[MESH] |Pneumonia, Viral/genetics/*immunology/pathology/virology[MESH] |Pulmonary Fibrosis/genetics/*immunology/pathology/virology[MESH] |SARS-CoV-2[MESH]SARS-CoV-2 triggers inflammatory responses and cell death through casp(epmc).pdf DeepDyve Pubget Overpricing