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Cellular senescence is not observed in some organisms, including perennial plants, sponges, corals, and lobsters. In other organisms, where cellular senescence is observed, cells eventually become post-mitotic: they can no longer replicate themselves through the process of cellular mitosis (i.e., cells
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.
The two theories; non-adaptive, and adaptive, are used to explain the evolution of senescence, which is the decline in reproduction with age. [8] The non-adaptive theory assumes that the evolutionary deterioration of human age occurs as a result of accumulation of deleterious mutations in the germline. [8]
One of the main criticisms of the free radical theory of aging is directed at the suggestion that free radicals are responsible for the damage of biomolecules, thus being a major reason for cellular senescence and organismal aging. [26]: 81 Several modifications have been proposed to integrate current research into the overall theory.
Although many models do illustrate an inverse relationship, and the theory makes sense from an evolutionary perspective, the cellular mechanisms have yet to be explored. However, with regards to cellular replication , the progressive shortening of telomeres is a mechanism which limits the amount of generations of a single cell may undergo . [ 10 ]
The repair model, instead of the target theory, emphasizes how a cell utilizes said cell’s repair mechanisms up to the limit of the cell’s repair machinery (the end of the shoulder). After the limit of the cell’s machinery is reached, the repair model generally notes that if any damage is left unhealed the dying process will be initiated.
A second study led by Jan van Deursen in collaboration with a team of collaborators at the Mayo Clinic and Groningen University, provided the first direct in vivo evidence that cellular senescence causes signs of aging by eliminating senescent cells from progeroid mice by introducing a drug-inducible suicide gene and then treating the mice with ...