tetano
Editor, Senior Moderator
Clin Immunol
. 2022 Aug 6;109093.
doi: 10.1016/j.clim.2022.109093. Online ahead of print.
Targeting autophagy regulation in NLRP3 inflammasome-mediated lung inflammation in COVID-19
Yuan-Yuan Yong[SUP] 1 [/SUP], Li Zhang[SUP] 1 [/SUP], Yu-Jiao Hu[SUP] 1 [/SUP], Jian-Ming Wu[SUP] 2 [/SUP], Lu Yan[SUP] 1 [/SUP], Yi-Ru Pan[SUP] 1 [/SUP], Yong Tang[SUP] 3 [/SUP], Lu Yu[SUP] 4 [/SUP], Betty Yuen-Kwan Law[SUP] 5 [/SUP], Chong-Lin Yu[SUP] 6 [/SUP], Jie Zhou[SUP] 1 [/SUP], Mao Li[SUP] 7 [/SUP], Da-Lian Qin[SUP] 8 [/SUP], Xiao-Gang Zhou[SUP] 9 [/SUP], An-Guo Wu[SUP] 10 [/SUP]
Affiliations
Abstract
Coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Emerging evidence indicates that the NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome is activated, which results in a cytokine storm at the late stage of COVID-19. Autophagy regulation is involved in the infection and replication of SARS-CoV-2 at the early stage and the inhibition of NLRP3 inflammasome-mediated lung inflammation at the late stage of COVID-19. Here, we discuss the autophagy regulation at different stages of COVID-19. Specifically, we highlighted the therapeutic potential of autophagy activators in COVID-19 by inhibiting the NLRP3 inflammasome, thereby avoiding the cytokine storm. We hope this review provides enlightenment for the use of autophagy activators targeting the inhibition of the NLRP3 inflammasome, specifically the combinational therapy of autophagy modulators with the inhibitors of the NLRP3 inflammasome, antiviral drugs, or anti-inflammatory drugs in the fight against COVID-19.
Keywords: Autophagy regulation; COVID-19; Lung inflammation; NLRP3 inflammasome; SARS-CoV-2.
. 2022 Aug 6;109093.
doi: 10.1016/j.clim.2022.109093. Online ahead of print.
Targeting autophagy regulation in NLRP3 inflammasome-mediated lung inflammation in COVID-19
Yuan-Yuan Yong[SUP] 1 [/SUP], Li Zhang[SUP] 1 [/SUP], Yu-Jiao Hu[SUP] 1 [/SUP], Jian-Ming Wu[SUP] 2 [/SUP], Lu Yan[SUP] 1 [/SUP], Yi-Ru Pan[SUP] 1 [/SUP], Yong Tang[SUP] 3 [/SUP], Lu Yu[SUP] 4 [/SUP], Betty Yuen-Kwan Law[SUP] 5 [/SUP], Chong-Lin Yu[SUP] 6 [/SUP], Jie Zhou[SUP] 1 [/SUP], Mao Li[SUP] 7 [/SUP], Da-Lian Qin[SUP] 8 [/SUP], Xiao-Gang Zhou[SUP] 9 [/SUP], An-Guo Wu[SUP] 10 [/SUP]
Affiliations
- PMID: 35944881
- DOI: 10.1016/j.clim.2022.109093
Abstract
Coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Emerging evidence indicates that the NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome is activated, which results in a cytokine storm at the late stage of COVID-19. Autophagy regulation is involved in the infection and replication of SARS-CoV-2 at the early stage and the inhibition of NLRP3 inflammasome-mediated lung inflammation at the late stage of COVID-19. Here, we discuss the autophagy regulation at different stages of COVID-19. Specifically, we highlighted the therapeutic potential of autophagy activators in COVID-19 by inhibiting the NLRP3 inflammasome, thereby avoiding the cytokine storm. We hope this review provides enlightenment for the use of autophagy activators targeting the inhibition of the NLRP3 inflammasome, specifically the combinational therapy of autophagy modulators with the inhibitors of the NLRP3 inflammasome, antiviral drugs, or anti-inflammatory drugs in the fight against COVID-19.
Keywords: Autophagy regulation; COVID-19; Lung inflammation; NLRP3 inflammasome; SARS-CoV-2.