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​英訳サンプル:       7​

Cellular senescence is a response of normal cells to potentially cancer-causing events.


複製セネッセンスとはセネッセンス細胞のサブセットであり、これが増殖中に停止すると細胞分裂数が多くなる(ヘイフリック限界では一般的に 40~60回の細胞分裂が生じる)。
The term replicative senescence identifies the subset of senescent cells whose arrest in proliferation is associated with their high number of cell divisions (the Hayflick limit – typically between 40 And 60 cell division).



The mechanism for replicative senescence involves each division resulting in a shortening of the telomere region of chromosomes such that a cumulative critical length is reached that does not support the DNA replication machinery.


Senescent cells exhibit an irreversible arrest of cell proliferation, an altered function and in some cases a resistance to apoptosis. Besides telomere shortening, inducers of senescence include DNA damage, oncogene expression, and supermitogenic signals and telomere-independent pathways which include: cytoskeletal, interferon-related, insulinlike growth factor (IGF)-related, MAP kinase and oxidative stress pathways.



The arrest in proliferation is imposed and maintained on cells by the induction of cyclin-dependent kinase inhibitors p16 and p21 that implement cell cycle arrest.


Senescent cells accumulate with age and at sites of age-related pathology. The senescent phenotype (e.g. secretion of IL-6) may be contributory to the pro-inflammatory state observed in normal aging and that is exacerbated in frailty.


The contribution of cellular (replicative) senescence to organismal aging has been controversial, though increasingly; evidence appears to link cellular senescence and aging.

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