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The negative implications of cellular senescence present themselves in the transition from acute to chronic senescence. When the immune system cannot clear senescent cells at the rate at which senescent cells are being produced, possibly as a result of the decline in immune function with age, accumulation of these cells leads to a disruption in ...
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:
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]
Often associated with aging and age-related diseases in vivo, senescent cells can be found in many renewable tissues, including the stroma, vasculature, hematopoietic system, and many epithelial organs. Resulting from accumulation over many cell divisions, senescence is often seen in age-associated degenerative phenotypes.
Aging of the immune system is a controversial phenomenon. Senescence refers to replicative senescence from cell biology, which describes the condition when the upper limit of cell divisions (Hayflick limit) has been exceeded, and such cells commit apoptosis or lose their functional properties.
Genetic theories of aging propose that aging is programmed within each individual's genes. According to this theory, genes dictate cellular longevity. Programmed cell death, or apoptosis, is determined by a "biological clock" via genetic information in the nucleus of the cell. Genes responsible for apoptosis provide an explanation for cell ...
Tumor necrosis factor (TNF) is increased 32-fold in stress-induced senescence, 8-fold in replicative senescence, and only slightly in proteosome-inhibited senescence. [9] Interleukin 6 (IL-6) and interleukin 8 (IL-8) are the most conserved and robust features of SASP. [10] But some SASP components are anti-inflammatory. [11]