SARS-CoV-2 targets the lysosome to mediate airway inflammatory cell death
Publication in refereed journal

替代計量分析
.

其它資訊
摘要As the coronavirus disease 2019 (COVID-19) pandemic continues to wreak havoc, researchers around the globe are working together to understand how the responsible agent - severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) damages the respiratory system and other organs. Macroautophagy/autophagy is an innate immune response against viral infection and is known to be manipulated by positive-strand RNA viruses, including SARS-CoV-2. Nevertheless, the link between autophagic subversion and cell death or inflammation in COVID-19 remains unclear. Emerging evidence suggests that SARS-CoV-2 could trigger pyroptosis, a form of inflammatory programmed cell death characterized by the activation of inflammasomes and CASP1 (caspase 1) and the formation of transmembrane pores by GSDMD (gasdermin D). In this connection, autophagic flux impairment is a known activator of inflammasomes. This prompted us to investigate if SARS-CoV-2 could target autophagy to induce inflammasome-dependent pyroptosis in lung epithelial cells.

Abbreviations: ATP6AP1: ATPase H+ transporting accessory protein 1; CASP1: caspase 1; COVID-19: coronavirus disease 2019; GSDMD: gasdermin D; IL1B: interleukin 1 beta; IL18: interleukin 18; KRT 18: keratin 18; NLRP3: NLR family pyrin domain containing 3; NOD: nucleotide oligomerization domain; NSP6: non-structural protein 6; TFEB: transcription factor EB; SARS-CoV-2: severe acute respiratory syndrome coronavirus 2
出版社接受日期17.12.2021
著者Xiao Sun, Jun Yu, Sunny Hei Wong, Matthew Tak Vai Chan, Lin Zhang, William Ka Kei Wu
期刊名稱Autophagy
出版年份2022
月份1
日期22
卷號18
期次9
頁次2246 - 2248
國際標準期刊號1554-8627
語言美式英語

上次更新時間 2024-20-08 於 00:29