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dc.creatorYaqinuddin, Ahmed
dc.creatorKashir, Junaid
dc.date.accessioned2020-07-15T20:11:41Z
dc.date.available2020-07-15T20:11:41Z
dc.date.created2020-10
dc.identifier.issn0306-9877spa
dc.identifier.otherhttps://www.sciencedirect.com/science/article/pii/S0306987720310215?via%3Dihubspa
dc.identifier.urihttp://hdl.handle.net/20.500.12010/10590
dc.format.extent4 páginasspa
dc.format.mimetypeapplication/pdfspa
dc.publisherScience Directeng
dc.sourcereponame:Expeditio Repositorio Institucional UJTLspa
dc.sourceinstname:Universidad de Bogotá Jorge Tadeo Lozanospa
dc.subjectSARSspa
dc.titleNovel therapeutic targets for SARS-CoV-2-induced acute lung injury: Targeting a potential IL-1β/neutrophil extracellular traps feedback loopspa
dc.type.localArtículospa
dc.subject.lembSíndrome respiratorio agudo gravespa
dc.subject.lembCOVID-19spa
dc.subject.lembSARS-CoV-2spa
dc.subject.lembCoronavirusspa
dc.rights.accessrightsinfo:eu-repo/semantics/openAccessspa
dc.type.hasversioninfo:eu-repo/semantics/acceptedVersionspa
dc.subject.keywordCOVID19spa
dc.subject.keywordCoronavirusspa
dc.subject.keywordInflammasomesspa
dc.subject.keywordNeutrophil extracellular traps (NETs)spa
dc.identifier.doihttps://doi.org/10.1016/j.mehy.2020.109906spa
dc.description.abstractenglishMost COVID-19 infected individuals present with mild flu-like symptoms; however, 5–10% of cases suffer from life-threatening pneumonia and respiratory failure. The pathogenesis of SARS-CoV-2 and its pathology of associated acute lung injury (ALI), acute respiratory distress syndrome (ARDS), sepsis, coagulopathy and multiorgan failure is not known. SARS-CoV-2 is an envelope virus with S (spike), M (membrane), N (nucleocapsid) and E (envelop) proteins. In a closely related coronavirus (SARS-CoV), the transmembrane E protein exerts an important role in membrane-ionic transport through viroporins, deletion of which reduced levels of IL-1β and a remarkably reduced lung edema compared to wild type. IL-1β is generated by macrophages upon activation of intracellular NLRP3 (NOD-like, leucine rich repeat domains, and pyrin domain-containing protein 3), part of the functional NLRP3 inflammasome complex that detects pathogenic microorganisms and stressors, while neutrophils are enhanced by increasing levels of IL-1β. Expiring neutrophils undergo “NETosis”, producing thread-like extracellular structures termed neutrophil extracellular traps (NETs), which protect against mild infections and microbes. However, uncontrolled NET production can cause acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), coagulopathy, multiple organ failure, and autoimmune disease. Herein, we present arguments underlying our hypothesis that IL-1β and NETs, mediated via NLRP3 inflammasomes, form a feed-forward loop leading to the excessive alveolar and endothelial damage observed in severe cases of COVID-19. Considering such assertions, we propose potential drug candidates that could be used to alleviate such pathologies. Considering that recent efforts to ascertain effective treatments of COVID-19 in severe patients has been less than successful, investigating novel avenues of treating this virus are essential.spa


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