Functional and tissue enrichment analyses suggest that SARS-CoV-2 infection affects host metabolism and catabolism mediated by interference on host proteins

Lopes, Luciano Rodrigo

doi:10.1007/s42770-021-00497-0

Cited by 1 publication

(1 citation statement)

References 79 publications

(90 reference statements)

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“…Besides, SARS-CoV-2 S protein can activate reactive oxygen species (ROS)-inhibited phosphoinositide 3-kinase (PI3K)/AKT/ mammalian target of rapamycin (mTOR) pathways, 39 subsequently inducing autophagy-triggered apoptosis and inflammation. 40 – 42 It is noteworthy that SARS-CoV-2 has weaker pro-apoptotic activity than SARS-CoV, 32 , 43 which may partially explain the more cases of asymptomatic patients with widespread viral transmission. Mutations of SARS-CoV-2 ORF3a attenuate cytosolic form-related apoptosis, whereas SARS-CoV ORF3a could well leverage this way.…”

Section: Apoptosis and Sars-cov-2mentioning

confidence: 99%

Cell deaths: Involvement in the pathogenesis and intervention therapy of COVID-19

Zhang

Wang

et al. 2022

Sig Transduct Target Ther

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The current pandemic of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has dramatically influenced various aspects of the world. It is urgent to thoroughly study pathology and underlying mechanisms for developing effective strategies to prevent and treat this threatening disease. It is universally acknowledged that cell death and cell autophagy are essential and crucial to maintaining host homeostasis and participating in disease pathogenesis. At present, more than twenty different types of cell death have been discovered, some parts of which have been fully understood, whereas some of which need more investigation. Increasing studies have indicated that cell death and cell autophagy caused by coronavirus might play an important role in virus infection and pathogenicity. However, the knowledge of the interactions and related mechanisms of SARS-CoV-2 between cell death and cell autophagy lacks systematic elucidation. Therefore, in this review, we comprehensively delineate how SARS-CoV-2 manipulates diverse cell death (including apoptosis, necroptosis, pyroptosis, ferroptosis, and NETosis) and cell autophagy for itself benefits, which is simultaneously involved in the occurrence and progression of COVID-19, aiming to provide a reasonable basis for the existing interventions and further development of novel therapies.

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