Concluding Remarks

The phenomenon of replicative senescence has been documented and characterized in cell culture for a variety of cell types. The basic phenotype of a senescent cell is a dysfunctional, permanently growth-arrested cell with reduced ability to undergo apoptosis. It is now clear that cells with similar characteristics do increase in frequency during aging, particularly within the immune system. However, analysis of T cell replicative senescence has led to a paradigm shift regarding the role of replicative senescence in organismic aging.

Early data showing correlations between in vitro cell growth and species lifespan had reinforced the notion that analysis of cells in culture would yield mechanistic insights into the process of aging. In hindsight, it appears that this goal might not have been realistic. It has become evident that senescent cells do affect lifespan, but probably not in the sense originally proposed. In other words, rather than affecting the basic aging process, senescent cells exert their impact on the aging organism by contributing to or enhancing certain age-related pathologies. Thus, senescent cells may affect lifespan only indirectly, not by modulating the rate of aging, but rather by affecting the risk of mortality. This altered view of the relationship between aging in cell culture and in vivo aging does not diminish the value of using cell culture models in the study of aging. It merely changes the hypotheses and interpretations of the experiments.

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