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COVID-19 and cellular senescence

Item Type:Article
Title:COVID-19 and cellular senescence
Creators Name:Schmitt, C.A. and Tchkonia, T. and Niedernhofer, L.J. and Robbins, P.D. and Kirkland, J.L. and Lee, S.
Abstract:The clinical severity of coronavirus disease 2019 (COVID-19) is largely determined by host factors. Recent advances point to cellular senescence, an ageing-related switch in cellular state, as a critical regulator of SARS-CoV-2-evoked hyperinflammation. SARS-CoV-2, like other viruses, can induce senescence and exacerbates the senescence-associated secretory phenotype (SASP), which is comprised largely of pro-inflammatory, extracellular matrix-degrading, complement-activating and pro-coagulatory factors secreted by senescent cells. These effects are enhanced in elderly individuals who have an increased proportion of pre-existing senescent cells in their tissues. SASP factors can contribute to a 'cytokine storm', tissue-destructive immune cell infiltration, endothelialitis (endotheliitis), fibrosis and microthrombosis. SASP-driven spreading of cellular senescence uncouples tissue injury from direct SARS-CoV-2-inflicted cellular damage in a paracrine fashion and can further amplify the SASP by increasing the burden of senescent cells. Preclinical and early clinical studies indicate that targeted elimination of senescent cells may offer a novel therapeutic opportunity to attenuate clinical deterioration in COVID-19 and improve resilience following infection with SARS-CoV-2 or other pathogens.
Source:Nature Reviews Immunology
ISSN:1474-1733
Publisher:Nature Publishing Group
Date:5 October 2022
Official Publication:https://doi.org/10.1038/s41577-022-00785-2
PubMed:View item in PubMed

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