dc.creator | Li, Shufen | |
dc.creator | Zhang, Yulan | |
dc.creator | Guan, Zhenqiong | |
dc.creator | Li, Huiling | |
dc.creator | Ye, Meidi | |
dc.creator | Chen, Xi | |
dc.creator | Shen, Jun | |
dc.creator | Zhou, Yiwu | |
dc.creator | Shi, Zheng-Li | |
dc.creator | Zhou1, Peng | |
dc.creator | Peng, Ke | |
dc.date.accessioned | 2020-10-14T15:52:09Z | |
dc.date.accessioned | 2022-09-23T18:32:48Z | |
dc.date.available | 2020-10-14T15:52:09Z | |
dc.date.available | 2022-09-23T18:32:48Z | |
dc.date.created | 2020-10-14T15:52:09Z | |
dc.identifier | 2059-3635 | |
dc.identifier | https://doi.org/10.1038/s41392-020-00334-0 | |
dc.identifier | http://hdl.handle.net/20.500.12010/14459 | |
dc.identifier | https://doi.org/10.1038/s41392-020-00334-0 | |
dc.identifier.uri | http://repositorioslatinoamericanos.uchile.cl/handle/2250/3502906 | |
dc.description.abstract | 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. | |
dc.language | eng | |
dc.publisher | Signal Transduction and Targeted Therapy | |
dc.rights | info:eu-repo/semantics/openAccess | |
dc.rights | Abierto (Texto Completo) | |
dc.source | reponame:Expeditio Repositorio Institucional UJTL | |
dc.source | instname:Universidad de Bogotá Jorge Tadeo Lozano | |
dc.subject | SARS-CoV-2 | |
dc.subject | Triggers inflammatory | |
dc.subject | Cell death | |
dc.subject | Caspase-8 | |
dc.title | SARS-CoV-2 triggers inflammatory responses and cell death through caspase-8 activation | |