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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:
Quiescent cells are often identified by low RNA content, lack of cell proliferation markers, and increased label retention indicating low cell turnover. [ 5 ] [ 6 ] Senescence is distinct from quiescence because senescence is an irreversible state that cells enter in response to DNA damage or degradation that would make a cell's progeny nonviable.
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.
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.
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 SASP in senescent neurons can vary according to cell type, the initiator of senescence, and the stage of senescence. [12] An online SASP Atlas serves as a guide to the various types of SASP. [8] SASP is one of the three main features of senescent cells, the other two features being arrested cell growth, and resistance to apoptosis. [13]