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Cell growth plays a crucial role in cell proliferation, regulating cellular homeostasis and cell cycle progression through dynamic changes in cell size. [1] And like DNA damage, it can promote senescence by triggering a prolonged cell cycle arrest. [5]
Senescence (/ s ɪ ˈ n ɛ s ə n s /) or biological aging is the gradual deterioration of functional characteristics in living organisms. Whole organism senescence involves an increase in death rates or a decrease in fecundity with increasing age, at least in the later part of an organism's life cycle.
Senescence can be induced by several factors, including telomere shortening, [37] DNA damage [38] and stress. Since the immune system is programmed to seek out and eliminate senescent cells, [39] it might be that senescence is one way for the body to rid itself of cells damaged beyond repair. The links between cell senescence and aging are several:
The typical normal human fetal cell will divide between 50 and 70 times before experiencing senescence. As the cell divides, the telomeres on the ends of chromosomes shorten. The Hayflick limit is the limit on cell replication imposed by the shortening of telomeres with each division. This end stage is known as cellular senescence.
Williams noted that senescence may be causing many deaths even if animals are not 'dying of old age.' [1] He began his hypothesis with the idea that ageing can cause earlier senescence due to the competitive nature of life. Even a small amount of ageing can be fatal; hence natural selection does indeed care and ageing is not cost-free. [17]
Senotherapeutic's refers to therapeutic agents/strategies that specifically target cellular senescence. [1] Senotherapeutic's include emerging senolytic/senoptotic small molecules that specifically induce cell death in senescent cells [2] and agents that inhibit the pro-inflammatory senescent secretome. [3]
Extending telomeres can allow cells to divide more and increase the risk of uncontrolled cell growth and cancer development. [24] A study conducted by Johns Hopkins University challenged the idea that long telomeres prevent aging. Rather than protecting cells from aging, long telomeres help cells with age-related mutations last longer. [13]
Therefore, a greater investment in growth and reproduction would result in reduced investment in DNA repair maintenance, leading to increased cellular damage, shortened telomeres, accumulation of mutations, compromised stem cells, and ultimately, senescence. Although many models, both animal and human, have appeared to support this theory ...