The role of cell death in SARS-CoV-2 infection

被引:10
|
作者
Yuan, Cui [1 ]
Ma, Zhenling [1 ]
Xie, Jiufeng [1 ]
Li, Wenqing [1 ]
Su, Lijuan [1 ]
Zhang, Guozhi [1 ]
Xu, Jun [1 ]
Wu, Yaru [1 ]
Zhang, Min [2 ]
Liu, Wei [1 ]
机构
[1] Henan Agr Univ, Coll Life Sci, Zhengzhou, Peoples R China
[2] Henan Univ Chinese Med, Coll Pharm, Zhengzhou, Peoples R China
基金
中国国家自然科学基金;
关键词
NLRP3; INFLAMMASOME; GASDERMIN-D; 7A PROTEIN; APOPTOSIS; FERROPTOSIS; ACTIVATION; PYROPTOSIS; COVID-19; NECROPTOSIS; NEUTROPHILS;
D O I
10.1038/s41392-023-01580-8
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), showing high infectiousness, resulted in an ongoing pandemic termed coronavirus disease 2019 (COVID-19). COVID-19 cases often experience acute respiratory distress syndrome, which has caused millions of deaths. Apart from triggering inflammatory and immune responses, many viral infections can cause programmed cell death in infected cells. Cell death mechanisms have a vital role in maintaining a suitable environment to achieve normal cell functionality. Nonetheless, these processes are dysregulated, potentially contributing to disease pathogenesis. Over the past decades, multiple cell death pathways are becoming better understood. Growing evidence suggests that the induction of cell death by the coronavirus may significantly contributes to viral infection and pathogenicity. However, the interaction of SARS-CoV-2 with cell death, together with its associated mechanisms, is yet to be elucidated. In this review, we summarize the existing evidence concerning the molecular modulation of cell death in SARS-CoV-2 infection as well as viral-host interactions, which may shed new light on antiviral therapy against SARS-CoV-2.
引用
收藏
页数:17
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