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

Yuan et al., Signal Transduction and Targeted Therapy, doi:10.1038/s41392-023-01580-8
Sep 2023  
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Review of cell death pathways in SARS-CoV-2 infection. Authors note that N-acetylcysteine (NAC) is a precursor to glutathione that may inhibit ferroptosis. Ferroptosis is a regulated cell death triggered by oxidative stress that has been implicated in COVID-19 pathogenesis. Through replenishing glutathione stores and reinforcing the glutathione peroxidase-4 pathway, NAC is suggested to potentially ameliorate ferroptosis in COVID-19.
See Schloss et al. for another review covering N-acetylcysteine for COVID-19.
Study covers selenium and N-acetylcysteine.
Yuan et al., 20 Sep 2023, peer-reviewed, 10 authors. Contact:
This PaperN-acetylcys..All
The role of cell death in SARS-CoV-2 infection
Cui Yuan, Zhenling Ma, Jiufeng Xie, Wenqing Li, Lijuan Su, Guozhi Zhang, Jun Xu, Yaru Wu, Min Zhang, Wei Liu
Signal Transduction and Targeted Therapy, doi:10.1038/s41392-023-01580-8
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.
AUTHOR CONTRIBUTIONS C.Y. and W.L. wrote the manuscript and created the figures. W.L. and Z.M. revised the manuscript and figures. J.X., W.L., L.S., G.Z., X.J., Y.W., and M.Z. provided conceptual ideas and revised the manuscript. All the authors have read and approved the final manuscript. ADDITIONAL INFORMATION Competing interests: The authors declare no competing interests. Figures were created with
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