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    Home > Biochemistry News > Biotechnology News > Nature magazine reports that COVID-19 will accelerate cell aging

    Nature magazine reports that COVID-19 will accelerate cell aging

    • Last Update: 2021-09-30
    • Source: Internet
    • Author: User
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    Since the outbreak of the new crown pneumonia, human understanding of the virus has been continuously updated
    .
    As a "flying disaster" of all mankind, its scope and scope of influence are getting bigger and bigger, and it profoundly affects the social order of mankind


    .


    Not only that, the new coronavirus (SARS-CoV-2), as a deadly virus, is also very harmful to infected patients
    .

    A study published in the medical journal Nature Medicine on June 23, 2021 shows that more than half of patients with mild new coronary pneumonia have difficulty breathing, loss of taste and smell, fatigue, and memory loss after 6 months of recovery.
    Symptoms
    .

    It is worth noting that after a cell is infected by a virus, it usually activates its own aging mechanism and rapidly declines
    .
    This is considered a way for the body to fight off viral infections


    .


    So, does SARS-CoV-2 infection also cause cell senescence? If so, how can we use this mechanism to fight the COVID-19 pandemic?

    On September 13, 2021, researchers from the Charité School of Medicine in Berlin, Germany, published a research paper entitled "Virus-induced senescence is driver and therapeutic target in COVID-19" in the journal Nature [2]
    .

    This study shows that after host cells are infected with the novel coronavirus (SARS-CoV-2), the mechanism of awakening their own cellular senescence is the main stress response
    .

    On this basis, the researchers used Senolytics therapy for senescent cells to selectively remove cells infected with the new coronavirus, thus proposing a new virus treatment plan
    .

     

     

    Virus infection can obviously cause cell damage and cause profound biological changes in the infected host cells, such as turning on the virus-triggered cell senescence switch
    .
    Virus-induced senescence (VIS) is no different from other forms of cellular senescence, and is accompanied by a secretory phenotype associated with senescence (SASP)


    .


     

    Senescence-related secretions are mainly composed of pro-inflammatory factors, extracellular matrix active factors, and procoagulant factors
    .
    They are also the basis of cytokine storms, macrophage activation, NET formation, endotheliitis, and widespread pulmonary thrombosis


    .


     

    From this perspective, virus-induced senescence (VIS) plays an important role in the development of new coronary pneumonia symptoms, and studying the relationship between the two may become the key to the treatment of patients with new coronary pneumonia
    .

     

    In this study, researchers found that COVID-19 patients with airway mucosa in situ aging markers and serum SASP factor levels increased
    .
    At the same time, in vitro experiments showed that COVID-19 patients manifested with macrophage activation, SASP-related secretion, and complement lysis, and SASP aggravated the secondary senescence of endothelial cells


    .


     

    This confirms that SARS-CoV-2, like other viruses, can also awaken cell senescence as the main stress response of infected cells
    .

     

    COVID-19 patients exhibit virus-induced senescence (VIS) characteristics

     

    So, how can virus-induced senescence (VIS) be applied to the treatment of COVID-19 patients?

     

    In 2015, a research team led by Dr.
    James Kirkland of the Mayo Clinic in the United States published a research paper on senescent cells [3], reporting a type of drug combination that selectively kills senescent cells Senolytics
    .

    Senolytics is composed of dasatinib and quercetin, which can selectively induce the death of senescent cells
    .
    Among them, dasatinib can eliminate aging human adipocyte progenitor cells, while quercetin can kill aging human endothelial cells and mouse bone marrow stem cells


    .


     

     

    On this basis, the research team tried to link the host cell senescence caused by SARS-CoV-2 with Senolytics and develop new targeted treatment strategies for COVID-19
    .

     

    The researchers constructed hamster and mouse models infected with SARS-CoV-2, and verified their conjecture by injecting a combination of Senolytics treatments such as Navitoclax and dasatinib/quercetin
    .
    They found that Senolytics can selectively eliminate virus-induced senescent cells, alleviate lung diseases related to COVID-19, and reduce inflammation


    .


     

    Senolytics treatment can alleviate COVID-19 disease characteristics in animal models and patients

     

    The author said: "The results of this study show that virus-induced senescence (VIS) is a key trigger for COVID-19-related cytokine upgrade and organ damage
    .
    Therefore, we believe that hemolysis targeting virus-infected cells is a new treatment Program to combat SARS-CoV-2 or other viral infections


    .


     

    VIS cells are sensitive to the targeting effect of Senolytics

     

    In conclusion, this study reveals that SARS-CoV-2 infection can also lead to stress-induced senescence of host cells
    .
    Therefore, Senolytics therapy for senescent cells can be used to eliminate SARS-CoV-2 infected cells and develop a new targeted therapy for COVID-19
    .

     

    In fact, this is not the first study linking Senolytics with COVID-19
    .
    On July 16, 2021, a research team from the University of Minnesota and the Mayo Medical Center published an article titled "Senolytics reduce coronavirus related mortality" in "Science" [4]
    .

    This study shows that the anti-aging drug Senolytics can reduce the death rate associated with coronavirus in elderly mice
    .

     

    references:

    1.
    https://
    2.
    https://
    3.
    https://onlinelibrary.
    wiley.
    com/doi/full/10.
    1111/acel.
    12344
    4.
    https://science.
    sciencemag.
    org//373/6552/eabe4832


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