2000
DOI: 10.1111/j.1749-6632.2000.tb06638.x
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Stress‐Induced Premature Senescence: Essence of Life, Evolution, Stress, and Aging

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Cited by 99 publications
(61 citation statements)
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“…In addition the age-related changes in morphology of serotonergic neurons in rat brain stem nuclei (Lolova 1996), frontal cortex, striatum, hypothalamus (Petkov et al 1987) and in various brain regions (Timiras et al 1984), decline in transport and uptake of tryptophan (Tang and Melethil 1995), melatonin and norepinephrine levels (Cardinali et al 2002) and MT 1 melatonin receptor in SCN (Wu et al 2007). The age induced decreased serotonin levels could also be responsible for age related increased MAO-B levels and neurodegeneration (Toussaint et al 2000). A similar change in neurotransmitter serotonin in hamsters could be responsible for decreased serotonin receptors 5-HT 7 and loss of sensitivity to the circadian effects of 8-OH-DPAT (serotonin agonist) and decreased density of a-adrenergic receptors in SCN with aging in hamster (Duncan et al 1999).…”
Section: Discussionmentioning
confidence: 97%
“…In addition the age-related changes in morphology of serotonergic neurons in rat brain stem nuclei (Lolova 1996), frontal cortex, striatum, hypothalamus (Petkov et al 1987) and in various brain regions (Timiras et al 1984), decline in transport and uptake of tryptophan (Tang and Melethil 1995), melatonin and norepinephrine levels (Cardinali et al 2002) and MT 1 melatonin receptor in SCN (Wu et al 2007). The age induced decreased serotonin levels could also be responsible for age related increased MAO-B levels and neurodegeneration (Toussaint et al 2000). A similar change in neurotransmitter serotonin in hamsters could be responsible for decreased serotonin receptors 5-HT 7 and loss of sensitivity to the circadian effects of 8-OH-DPAT (serotonin agonist) and decreased density of a-adrenergic receptors in SCN with aging in hamster (Duncan et al 1999).…”
Section: Discussionmentioning
confidence: 97%
“…This is particularly true if the senescent phenotype is directly linked to DNA damage, as in the case of progressive/stress-induced senescence (in contrast to replicative senescence, which is mainly caused by chromosomal instability due to telomere shortening) after repetitive cell duplication 9,10 . A chaotic gene expression pattern on the cellular level appears to be one potentially important facet of chondrocyte behavior in OA cartilage 7,8 , though this has never been investigated systematically in the tissue.…”
Section: Introductionmentioning
confidence: 99%
“…This type of senescence is now known to result from the DNA damage response (DDR) due to telomere shortening. 5 Stress-induced premature senescence of normal cells 3,6 results from responses to stresses, such as oxidative stress, Cells undergo senescence in response to various conditions, including telomere erosion, oncogene activation and multiple cytokines. one of these cytokines, interleukin-6 (IL-6), not only functions in the immune system, but also promotes cellular senescence and cancer.…”
Section: Introductionmentioning
confidence: 99%