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  1. 1001
  2. 1002
    “…Sirtuin family members with lysine deacetylase activity are known to play an important role in anti-aging and longevity. Cellular senescence is one of the hallmarks of aging, and downregulation of sirtuin is reported to induce premature senescence. …”
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  3. 1003
    “…Cellular senescence plays an important role in diverse biological processes such as tumorigenesis and organismal aging. …”
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  4. 1004
    “…Cellular senescence is a stress response to a variety of extrinsic and intrinsic insults that cause genomic or epigenomic perturbations. …”
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  5. 1005
    “…Although increasing evidence has documented the metabolic changes in senescent cells, mitochondrial function and its potential contribution to the fate of senescent cells remain largely unknown. …”
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  6. 1006
    por Guerrero, Ana, Gil, Jesús
    Publicado 2016
    “…The senescence-associated secretory phenotype (SASP) is a hallmark of senescence with an important physiological impact, but how it is established is unclear. …”
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  7. 1007
    “…Cellular senescence, a form of cell cycle arrest, is one of the cellular responses to different types of exogenous and endogenous damage. …”
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  8. 1008
    “…In cold extracts of senescent leaves of the plum tree (Prunus domestica ssp. domestica), six colorless non‐fluorescent chlorophyll catabolites (NCCs) were characterized, named Pd‐NCCs. …”
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  9. 1009
    “…Aging (senescence) includes causal mechanisms (etiologies) of late-life disease, which remain poorly understood. …”
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  10. 1010
    “…Here, we formally study how telomere shortening mechanisms impact on senescence kinetics and define two regimes of senescence, depending on the initial telomere length variance. …”
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  11. 1011
  12. 1012
    “…In addition, activated transcription and loss of centromeres identity are features of permanently arrested senescent cells with persistent DDR activation. Together, these findings bring out cooperation between DDR effectors and loss of centromere integrity as a safeguard mechanism to prevent genomic instability in context of persistent DNA damage signalling.…”
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  13. 1013
    “…The evolution of senescence is often explained by arguing that, in nature, few individuals survive to be old and hence it is evolutionarily unimportant what happens to organisms when they are old. …”
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  14. 1014
    “…Copper sulfate-induced premature senescence (CuSO(4)-SIPS) consistently mimetized molecular mechanisms of replicative senescence, particularly at the endoplasmic reticulum proteostasis level. …”
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  15. 1015
    “…We examined 16 Miscanthus genotypes with different flowering and senescence times for variation in N, P, K, moisture, ash, Cl and Si contents, hypothesizing that early flowering and senescence could result in improved biomass quality and/or enable an earlier harvest of biomass (in autumn at peak yield). …”
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  16. 1016
    “…We herein propose that the ability of senescence-associated inflammatory signaling to regulate in vivo reprogramming cycles of tissue repair outlines a threshold model of aging and cancer. …”
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  17. 1017
    “…However, the senescence-associated secretory phenotype (SASP) of senescent cells can promote tumorigenesis. …”
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  18. 1018
    “…Glioblastomas have a high frequency of mutations in the TERT promoter and CDKN2A locus that are expected to render them resistant to both replicative and oncogene-induced senescence. However, exposure of PriGO8A primary glioblastoma cells to media with 10% serum induced a senescence-like phenotype characterized by increased senescence-associated β galactosidase activity, PML bodies and p21 and morphological changes typical of senescence. …”
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  19. 1019
    “…However, the importance of miRNAs in regulating OS in the context of aging and cellular senescence is largely unknown. The purpose of our article is to highlight recent advancements in the regulatory role of miRNAs in OS-induced cellular senescence.…”
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  20. 1020
    “…Paradoxical observations have been made regarding the role of caveolin‐1 (Cav‐1) during cellular senescence. For example, caveolin‐1 deficiency prevents reactive oxygen species‐induced cellular senescence despite mitochondrial dysfunction, which leads to senescence. …”
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