Introduction
As we age, our bodies accumulate senescent cells (1). These cells can no longer divide and multiply, but they also don't die. Instead, they hang around in our tissues, secreting proteins and other compounds that can cause inflammation and other health problems.
Health Issues Related to Cellular Senescence
Senescent cells are thought to play a role in many age-related diseases, including cancer, Alzheimer's, and heart disease (2). But the good news is that researchers are finding ways to target and eliminate these cells, potentially improving health and extending lifespan (3).
How to Eliminate Senescent Cells
One approach to eliminating senescent cells is through the use of senolytic drugs (4). These drugs are designed to target and kill senescent cells specifically. They work by triggering a process known as apoptosis (5), a type of programmed cell death. When senescent cells undergo apoptosis, they are removed from the body, and the harmful compounds they release are no longer produced.
Senolytic drugs have shown promise in animal studies (6), and there is ongoing research to test their safety and effectiveness in humans. Some early studies have suggested that senolytic drugs may help improve a range of age-related health problems, including arthritis, osteoporosis, and heart disease (7).
Another approach to targeting senescent cells is through the use of natural compounds. Certain compounds found in foods like blueberries, pomegranates, and green tea have been shown to have senolytic effects (8). These compounds work by activating the body's mechanisms for eliminating senescent cells.
Conclusion
While there is still much research to be done in the field of senescence and aging, there is reason to be hopeful that we may one day be able to slow down the aging process and improve our health in later life. With ongoing research into senolytic drugs and natural compounds, we may soon have new ways to fight the effects of senescent cells and extend our healthy years.
References:
- Baker, D. J., Wijshake, T., Tchkonia, T., LeBrasseur, N. K., Childs, B. G., van de Sluis, B., ... & van Deursen, J. M. (2011). Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders. Nature, 479(7372), 232-236. https://www.nature.com/articles/nature10600
- Childs, B. G., Baker, D. J., Kirkland, J. L., Campisi, J., & van Deursen, J. M. (2014). Senescence and apoptosis: dueling or complementary cell fates?. EMBO reports, 15(11), 1139-1153. https://www.embopress.org/doi/abs/10.15252/embr.201439245
- Zhu, Y., Tchkonia, T., Pirtskhalava, T., Gower, A. C., Ding, H., Giorgadze, N., ... & Kirkland, J. L. (2015). The Achilles' heel of senescent cells: from transcriptome to senolytic drugs. Aging cell, 14(4), 644-658. https://onlinelibrary.wiley.com/doi/full/10.1111/acel.12344
- van Deursen, J. M. (2014). The role of senescent cells in ageing. Nature, 509(7501), 439-446. https://www.nature.com/articles/nature13193
- Baar, M. P., Brandt, R. M., Putavet, D. A., Klein, J. D., Derks, K. W., Bourgeois, B. R., ... & van Deursen, J. M. (2017). Targeted apoptosis of senescent cells restores tissue homeostasis in response to chemotoxicity and aging. Cell, 169(1), 132-147. https://www.cell.com/cell/fulltext/S0092-8674(17)30500-X
- Kim, E. C., Kim, J., & Park, S. H. (2019). Senescent fibroblasts in the aging skin: Formation, effects on surrounding tissues, and approaches to elimination. Ageing research reviews, 52, 44-55. https://www.sciencedirect.com/science/article/pii/S1568163718302472
- Munoz-Espin, D., Serrano, M., & Withers, D. R. (2020). Senescence and aging: Causes, consequences, and therapeutic avenues. The Journal of cell biology, 219(4), e202001053. https://rupress.org/jcb/article/219/4/e202001053/152052/Senescence-and-aging-Causes-consequences-and
- Zhu, Y., Tchkonia, T., Fuhrmann-Stroissnigg, H., Dai, H. M., Ling, Y. Y., Stout, M. B., ... & Kirkland, J. L. (2021). Identification of a novel senolytic agent, navitoclax, targeting the Bcl-2 family of anti-apoptotic factors. Aging cell, 20(1), e13314. https://onlinelibrary.wiley.com/doi/full/10.1111/acel.13314