COVID-19 promotes cellular senescence leading to long-term sequelae

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Nature Aging: COVID-19 promotes cellular senescence leading to long-term sequelae

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Nature Aging: COVID-19 promotes cellular senescence leading to long-term sequelae.

Since the COVID-19 pandemic began in December 2019, more than 200 million people worldwide have been infected with COVID-19, resulting in more than 5 million deaths.

In addition, a large proportion of people infected with the COVID-19 still have long-term sequelae even after recovery, which is also called ” Long COVID” .

Therefore, a deeper understanding of the biological response after SARS-CoV-2 infection, especially the persistent response, is needed.

Since COVID-19 tends to be more severe in older adults, there may be an important link between COVID-19 infection and aging.

Cellular senescence is an irreversible cell cycle state arrest that can be induced by a variety of potentially oncogenic stimuli and is considered a tumor suppressor mechanism.

Unlike apoptotic cells, senescent cells do not die immediately, but accumulate throughout the body. Importantly, senescent cells are not only non-dividing, they also develop a cellular senescence-associated secretory phenotype (SASP) .

In this phenomenon, senescent cells secrete a variety of pro-inflammatory factors, such as inflammatory cytokines, chemokines, growth factors, and extracellular matrix-degrading enzymes, among others.

Thus, although the induction of cellular senescence primarily acts as a tumor suppressor, the excessive accumulation of senescent cells in vivo due to senescence can adversely affect cellular senescence-associated secretory phenotype (SASP) .

And studies have shown that genetically or pharmacologically removing senescent cells can slow the onset of aging-related inflammatory diseases in aged mice.

Recently, a research team from Osaka University in Japan published a research paper titled: SARS-CoV-2 infection triggers paracrine senescence and leads to a sustained senescence-associated inflammatory response in Nature Aging , a sub-journal of Nature [1].

The study shows that SARS-CoV-2 infects cells and induces a cellular senescence-associated secretory phenotype (SASP) , which affects nearby uninfected cells to experience senescence-like cell cycle arrest, and this effect persists even after SARS-CoV-2 is cleared. .

This suggests to us that the cellular senescence-associated secretory phenotype (SASP) caused by 2019-nCoV infection may be the cause of ” Long COVID ” .

Prior to this, on July 16, 2021, a research team from the University of Minnesota and Mayo Medical Center published a research paper in the journal Science entitled: Senolytics reduce coronavirus-related mortality in old mice [2] . The study showed that the anti-aging drug Senolytics was able to reduce coronavirus-related mortality in aged mice .

On September 13, 2021, researchers from the Charité School of Medicine in Berlin, Germany published a research paper titled: Virus-induced senescence is driver and therapeutic target in COVID-19 in Nature [ 3] .

This study shows that host cells wake up their own cellular senescence mechanisms as a major stress response after being infected with the new coronavirus .

Based on this, the researchers used Senolytics therapy against senescent cells to selectively remove cells infected with the new coronavirus, thereby revealing a new viral treatment option.

In the new study, the research team found that cells infected with SARS-CoV-2 develop a cellular senescence-associated secretory phenotype (SASP) , which in turn triggers senescence-like cell cycle arrest in nearby cells.

In cultured human cells or bronchial organoids, these SARS-CoV-2-induced senescent cells continued to express high levels of a series of inflammatory factors, the so-called cellular senescence-associated secretory phenotype (SASP) , even after SARS-CoV-2 was cleared. , this senescence-associated secretory phenotype also persists.

The study also found increased gene expression of the senescence marker CDKN2A and various cellular senescence-associated secretory phenotype (SASP) factors in acellular cells of many Covid-19 survivors with sequelae .

In addition, mouse experiments found that the mouse model infected with the COVID-19 showed the phenomenon of cellular senescence and cellular senescence-associated secretory phenotype (SASP) 14 days after infection, which persisted even when the new coronavirus could not be detected. , while the use of anti-aging drugs such as Senolytics can reduce cellular senescence and SASP phenomena.

Collectively, this study shows that SARS-CoV-2 infects cells and induces a cellular senescence-associated secretory phenotype (SASP) , thereby affecting senescence-like cell cycle arrest in nearby uninfected cells, and this effect occurs even after SARS-CoV- 2. persisted after being cleared.

This suggests to us that the cellular senescence-associated secretory phenotype (SASP) caused by 2019-nCoV infection may be the cause of ” Long COVID ” .

Reference :
https://www.nature.com/articles/s43587-022-00170-7
https://science.sciencemag.org//373/6552/eabe4832
https://www.nature.com/articles/s41586-021-03995-1

Nature Aging: COVID-19 promotes cellular senescence leading to long-term sequelae

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