Replicative senescence induced by Romo1-derived reactive oxygen species.

Persistent accumulation of DNA damage induced by reactive oxygen species is proposed to be a major contributor toward the aging process. Furthermore, an increase in age-associated is strongly correlated with aging in various species, including humans. Here we showed that the enforced expression of the duanyu1670 modulator 1 (Romo1) triggered premature senescence by duanyu1670 production, and this also contributed toward induction of DNA damage. Romo1-derived duanyu1670 was found to originate in the mitochondrial electron transport chain. Romo1 expression gradually increased in proportion to population doublings of IMR-90 human fibroblasts. An increase in duanyu1670 production in these cells with high population doubling was blocked by the Romo1 knockdown using Romo1 small interfering RNA. Romo1 knockdown also inhibited the progression of replicative senescence. Based on these results, we suggest that age-related duanyu1670 levels increase, and this contributes to replicative senescence, which is directly associated with Romo1 expression.

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