Cell deaths: Involvement in the pathogenesis and intervention therapy of COVID-19
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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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Certain cytokines such as IL-1β and IL-6 have clearly emerged as key to promoting inflammaging.
“Certain cytokines, such as IL-1β and IL-6, have clearly emerged as key to promoting inflammaging.83,229–232”
From Inflammation and aging: signaling pathways and intervention therapies (2023) · cites this paper as [229]
In “Pyroptosis during SARS-CoV-2 infection” (page not provided), the paper identifies IL-1β and IL-6 as pro-inflammatory cytokines and says these mediators intensify inflammation and tissue damage. That discussion concerns COVID-19, not inflammaging, so it does not establish their claimed role in promoting inflammaging. (LLM, conf=0.82)
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- Authors
- Li, X., Zhang, Z., Wang, Z., Gutiérrez-Castrellón, P., & Shi, H.
- Affiliations
- Sichuan University (CN)
- Venue
- Signal Transduction and Targeted Therapy
- Published
- 2022-06-13
- Volume
- 7
- Issue
- 1
- Pages
- 186-186
- ISSN
- 2059-3635 (ISSN-L)
- PMC
- PMC9189267
- OpenAlex
- W4282575739
- Cited by
- 67
- References
- 327
- Citations by year
- 2026: 6 · 2025: 14 · 2024: 18 · 2023: 24 · 2022: 4
- FWCI
- 1.56
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Signal Transduction and Targeted Therapy (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- National Natural Science Foundation of China (81201788)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Health Sciences › Medicine › Infectious Diseases › SARS-CoV-2 and COVID-19 Research
- Keywords
- COVID-19 pandemic, SARS-CoV-2, cell death, autophagy, apoptosis, necroptosis, pyroptosis, ferroptosis, NETosis, viral pathogenesis, antiviral therapy
- MeSH terms
- COVID-19, SARS-CoV-2, Autophagy, Humans, Apoptosis, Pandemics
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