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- W4303024505 endingPage "104299" @default.
- W4303024505 startingPage "104299" @default.
- W4303024505 abstract "A hyperinflammatory response during severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection crucially worsens clinical evolution of coronavirus disease 2019 (COVID-19). The interaction between SARS-CoV-2 and angiotensin-converting enzyme 2 (ACE2) triggers the activation of the NACHT, leucine-rich repeat, and pyrin domain-containing protein 3 (NLRP3) inflammasome. Enhanced inflammasome activity has been associated with increased disease severity and poor prognosis. Evidence suggests that inflammasome activation and interleukin-1β (IL-1β) release aggravate pulmonary injury and induce hypercoagulability, favoring progression to respiratory failure and widespread thrombosis eventually leading to multiorgan failure and death. Observational studies with the IL-1 blockers anakinra and canakinumab provided promising results. In the SAVE-MORE trial, early treatment with anakinra significantly shortened hospital stay and improved survival in patients with moderate-to-severe COVID-19. In this review, we summarize current evidence supporting the pathogenetic role of the NLRP3 inflammasome and IL-1β in COVID-19, and discuss clinical trials testing IL-1 inhibition in COVID-19." @default.
- W4303024505 created "2022-10-07" @default.
- W4303024505 creator A5024558870 @default.
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- W4303024505 creator A5082299364 @default.
- W4303024505 date "2022-11-01" @default.
- W4303024505 modified "2023-10-18" @default.
- W4303024505 title "Interleukin-1 and the NLRP3 inflammasome in COVID-19: Pathogenetic and therapeutic implications" @default.
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