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  2. Cellular senescence - Wikipedia

    en.wikipedia.org/wiki/Cellular_senescence

    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

  3. Hallmarks of aging - Wikipedia

    en.wikipedia.org/wiki/Hallmarks_of_aging

    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:

  4. G0 phase - Wikipedia

    en.wikipedia.org/wiki/G0_phase

    [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. Such DNA damage can occur from telomere shortening over many cell divisions as well as reactive oxygen species (ROS) exposure, oncogene activation, and ...

  5. Evolution of ageing - Wikipedia

    en.wikipedia.org/wiki/Evolution_of_ageing

    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]

  6. Hayflick limit - Wikipedia

    en.wikipedia.org/wiki/Hayflick_limit

    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.

  7. Free-radical theory of aging - Wikipedia

    en.wikipedia.org/wiki/Free-radical_theory_of_aging

    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.

  8. Disposable soma theory of aging - Wikipedia

    en.wikipedia.org/wiki/Disposable_soma_theory_of...

    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]

  9. Antagonistic pleiotropy hypothesis - Wikipedia

    en.wikipedia.org/wiki/Antagonistic_pleiotropy...

    Strength of natural selection plot as a function of age. The antagonistic pleiotropy hypothesis (APT) is a theory in evolutionary biology that suggests certain genes may confer beneficial effects early in an organism's life, enhancing reproductive success, while also causing detrimental effects later in life, contributing to the aging process.