AI Article Synopsis

  • - The WHO reports around 41 million annual deaths globally from age-related non-communicable chronic diseases, highlighting the need for strategies to manage cell senescence and aging.
  • - Cell senescence contributes to aging-related dysfunction; researchers are investigating existing anticancer drugs for their potential to treat senescence and improve lifespan in animal studies.
  • - Senomorphics aim to restore healthy cellular functions, while senolytics induce the death of senescent cells, potentially leading to new treatments for chronic diseases based on these properties.

Article Abstract

The WHO estimated around 41 million deaths worldwide each year for age-related non-communicable chronic diseases. Hence, developing strategies to control the accumulation of cell senescence in living organisms and the overall aging process is an urgently needed problem of social relevance. During aging, many biological processes are altered, which globally induce the dysfunction of the whole organism. Cell senescence is one of the causes of this modification. Nowadays, several drugs approved for anticancer therapy have been repurposed to treat senescence, and others are under scrutiny in vitro and in vivo to establish their senomorphic or senolytic properties. In some cases, this research led to a significant increase in cell survival or to a prolonged lifespan in animal models, at least. Senomorphics can act to interfere with a specific pathway in order to restore the appropriate cellular function, preserve viability, and to prolong the lifespan. On the other hand, senolytics induce apoptosis in senescent cells allowing the remaining non-senescent population to preserve or restore tissue function. A large number of research articles and reviews recently addressed this topic. Herein, we would like to focus attention on those chemical agents with senomorphic or senolytic properties that perspectively, according to literature, suggest a potential application as senotherapeutics for chronic diseases.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7663758PMC
http://dx.doi.org/10.3390/ijms21217984DOI Listing

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