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Oxidative stress shortens telomeres.
Telomeres in most human cells shorten with each round of DNA replication, because they lack the enzyme telomerase. This is not, however, the only determinant of the rate of loss of telomeric DNA.Expand
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Feedback between p21 and reactive oxygen production is necessary for cell senescence
Cellular senescence—the permanent arrest of cycling in normally proliferating cells such as fibroblasts—contributes both to age‐related loss of mammalian tissue homeostasis and acts as a tumourExpand
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Fat tissue, aging, and cellular senescence
Fat tissue, frequently the largest organ in humans, is at the nexus of mechanisms involved in longevity and age‐related metabolic dysfunction. Fat distribution and function change dramaticallyExpand
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Chronic inflammation induces telomere dysfunction and accelerates ageing in mice
Chronic inflammation is associated with normal and pathological ageing. Here we show that chronic, progressive low-grade inflammation induced by knockout of the nfkb1 subunit of the transcriptionExpand
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A senescent cell bystander effect: senescence-induced senescence
Senescent cells produce and secrete various bioactive molecules including interleukins, growth factors, matrix‐degrading enzymes and reactive oxygen species (ROS). Thus, it has been proposed thatExpand
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Health and disease in 85 year olds: baseline findings from the Newcastle 85+ cohort study
Objectives The Newcastle 85+ Study aims to systematically study the clinical, biological, and psychosocial attributes of an unselected cohort of 85 year olds and to examine subsequent healthExpand
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Mitochondrial Dysfunction Accounts for the Stochastic Heterogeneity in Telomere-Dependent Senescence
Aging is an inherently stochastic process, and its hallmark is heterogeneity between organisms, cell types, and clonal populations, even in identical environments. The replicative lifespan of primaryExpand
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Mild hyperoxia shortens telomeres and inhibits proliferation of fibroblasts: a model for senescence?
Mild oxidative stress as exerted by culture of human WI-38 fibroblasts under 40% oxygen partial pressure blocks proliferation irreversibly after one to three population doublings. HyperoxicallyExpand
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Mitochondria are required for pro‐ageing features of the senescent phenotype
Cell senescence is an important tumour suppressor mechanism and driver of ageing. Both functions are dependent on the development of the senescent phenotype, which involves an overproduction ofExpand
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Postmitotic neurons develop a p21-dependent senescence-like phenotype driven by a DNA damage response
In senescent cells, a DNA damage response drives not only irreversible loss of replicative capacity but also production and secretion of reactive oxygen species (ROS) and bioactive peptides includingExpand
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