Cellular senescence as a potential mediator of COVID‐19 severity in the elderly
Open accessAbstract
SARS‐CoV‐2 is a novel betacoronavirus which infects the lower respiratory tract and can cause coronavirus disease 2019 (COVID‐19), a complex respiratory distress syndrome. Epidemiological data show that COVID‐19 has a rising mortality particularly in individuals with advanced age. Identifying a functional association between SARS‐CoV‐2 infection and the process of biological aging may provide a tractable avenue for therapy to prevent acute and long‐term disease. Here, we discuss how cellular senescence—a state of stable growth arrest characterized by pro‐inflammatory and pro‐disease functions—can hypothetically be a contributor to COVID‐19 pathogenesis, and a potential pharmaceutical target to alleviate disease severity. First, we define why older COVID‐19 patients are more likely to accumulate high levels of cellular senescence. Second, we describe how senescent cells can contribute to an uncontrolled SARS‐CoV‐2‐mediated cytokine storm and an excessive inflammatory reaction during the early phase of the disease. Third, we discuss the various mechanisms by which senescent cells promote tissue damage leading to lung failure and multi‐tissue dysfunctions. Fourth, we argue that a high senescence burst might negatively impact on vaccine efficacy. Measuring the burst of cellular senescence could hypothetically serve as a predictor of COVID‐19 severity, and targeting senescence‐associated mechanisms prior and after SARS‐CoV‐2 infection might have the potential to limit a number of severe damages and to improve the efficacy of vaccinations.
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Endothelial senescence may underlie the enhanced prothrombotic properties of injured endothelium in COVID-19 by shifting the balance between anti- and procoagulant pathways.
“Endothelial senescence may underlie the enhanced prothrombotic properties of injured endothelium in COVID-19 by shifting the balance between anti- and procoagulant pathways (63).”
From Lung epithelial and endothelial damage, loss of tissue repair, inhibition of fibrinolysis, and cellular senescence in fatal COVID-19 (2021) · cites this paper as [63]
SASP modulators are being trialled to reduce mortality in hospitalised COVID-19 patients due to potential in repressing cytokine storm.
“SASP modulators are actively being trialled to reduce mortality in hospitalised COVID‐19 patients, owing to their potential in repressing the detrimental cytokine storm (Nehme et al, 2020).”
From The struggle of a good friend getting old: cellular senescence in viral responses and therapy (2021) · cites this paper as Nehme et al, 2020
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- Authors
- Nehme, J., Borghesan, M., Mackedenski, S., Bird, T. G., & Demaria, M.
- Affiliations
- University Medical Center Groningen (NL)
- Cancer Research UK Scotland Institute (GB)
- Corresponding author
- Demaria, Marco
- Venue
- Aging Cell
- Publisher
- Wiley
- Published
- 2020-09-21
- Volume
- 19
- Issue
- 10
- Pages
- e13237-e13237
- ISSN
- 1474-9718 (ISSN-L)
- 1474-9726
- PMC
- PMC7576296
- OpenAlex
- W3087257480
- Cited by
- 94
- References
- 151
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 13 · 2023: 16 · 2022: 25 · 2021: 33 · 2020: 2
- FWCI
- 2.42
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Aging Cell (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Edinburgh Research Explorer (University of Edinburgh) (acceptedVersion, cc-by)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (submittedVersion, cc-by)
- Funders
- Wellcome Trust (107492/Z/15/Z)
- Cancer Research UK (26813)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Infectious Diseases › COVID-19 Clinical Research Studies
- Health Sciences › Medicine › Infectious Diseases › SARS-CoV-2 and COVID-19 Research
- Keywords
- cellular senescence, COVID-19 pandemic, SARS-CoV-2, older adults, disease severity, cytokine storm, inflammation, respiratory failure, tissue damage, vaccine efficacy, biological aging, senolytics
- MeSH terms
- Betacoronavirus, COVID-19, SARS-CoV-2, Age Factors, Aged, Aging, Humans, Pneumonia, Viral, Severity of Illness Index, Biomarkers, Cellular Senescence, Coronavirus Infections, Pandemics
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