Systems-Level Modelling Of DNA Damage, Senescence, And Stem Cell Dynamics In Ageing
Aging is a complex process involving many changes at the cellular level that increase our vulnerability to diseases. A major factor in this process is “cellular senescence,” which is when cells stop dividing permanently due to stress, such as damage to their DNA. These senescent cells can accumulate and contribute to aging.
Understanding how these intricate mechanisms interact has been challenging with traditional lab methods. However, a recent study introduces a powerful new mathematical model that simulates the dynamics of cellular aging within a population of cells. This model incorporates crucial processes like DNA repair, the state of cellular inactivity (“quiescence”), programmed cell death (“apoptosis”), and cell division.
By using this model, researchers can simulate the effects of aging and test the effectiveness of various interventions. For example, they can evaluate “senolytics” (drugs designed to eliminate senescent cells), strategies to preserve “telomere length” (the protective caps on our chromosomes that shorten with age), and stem cell therapies. The simulations accurately reproduce key features of aging, such as the gradual buildup of senescent cells and the limited number of times cells can divide before becoming senescent, known as “Hayflick limits.”
This innovative model provides a quantitative platform for testing hypotheses and identifying which anti-aging interventions are most promising for further experimental validation. It offers a predictive framework to better understand cellular aging and guide future research.
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