ライフサイエンスコーパス: cellular aging

1 ach far into later adulthood in part through cellular aging.

2 of mitochondrial biogenesis are involved in cellular aging.

3 yte telomere length (LTL) as an indicator of cellular aging.

4 gy are each associated with these markers of cellular aging.

5 ormed our understanding of the mechanisms of cellular aging.

6 relative telomere length (RTL), a marker of cellular aging.

7 iates oxidative stress (OXS) and accelerates cellular aging.

8 a on inflammaging and molecular processes of cellular aging.

9 mulation of mitochondria occurs often during cellular aging.

10 n maintaining telomere length and preventing cellular aging.

11 ans, and have implications for understanding cellular aging.

12 t hostility might impact health by promoting cellular aging.

13 ogens may be associated with deceleration of cellular aging.

14 These effects may be mediated by accelerated cellular aging.

15 Protein damage contributes prominently to cellular aging.

16 ssing mechanism and a commonly used model of cellular aging.

17 o the ends of linear chromosomes and retards cellular aging.

18 te as the sole factor impacting the tempo of cellular aging.

19 ess impacts health by modulating the rate of cellular aging.

20 motes cell growth and survival and may delay cellular aging.

21 of these pathways, involving Snf1, regulates cellular aging.

22 Oxidative damage plays a central role in cellular aging.

23 e our understanding of growth regulation and cellular aging.

24 anisms and validate the system as a model of cellular aging.

25 s (MSCs) recapitulates features of premature cellular aging, a global loss of H3K9me3, and changes in

26 ate that depressed patients show accelerated cellular aging according to a 'dose-response' gradient:

27 ecies on DNA and that this may contribute to cellular aging, age-related pathologies, and tumorigenes

28 mitochondrial decay with oxidant leakage and cellular aging and are associated with late onset diseas

29 NA G-quadruplex arrangements are involved in cellular aging and cancer, thus boosting the discovery o

30 nuclear phospho-Akt and telomerase delaying cellular aging and death.

31 ipid peroxidation, is a central component of cellular aging and is thought to play a role in the path

32 proteins are involved in DNA recombination, cellular aging and maintenance of genome stability.

33 unwanted proteins contributes prominently to cellular aging and neurodegeneration.

34 stem cell aging as the possible link between cellular aging and organismal aging.

35 s protect chromosome ends and are markers of cellular aging and replicative capacity.

36 ude that fission yeast does not age and that cellular aging and replicative lifespan can be uncoupled

37 f angiogenesis in the skin, the influence of cellular aging and replicative senescence (i.e., the ina

38 in part on whether the procedure can reverse cellular aging and restore somatic cells to a phenotypic

39 ermine whether IGF2 imprinting is altered in cellular aging and senescence, human prostate epithelial

40 Cellular aging and the development of replicative senesc

41 ole in the control of cell fate inheritance, cellular aging, and rejuvenation, i.e., the resetting of

42 Telomeres play a central role in cellular aging, and shorter telomere length has been ass

43 key molecular process can directly influence cellular aging, and thus could provide guidance for the

44 of telomere attrition, a potential marker of cellular aging, are not well understood.

45 leukocyte telomere length (LTL), a marker of cellular aging, are poorly understood.

46 s linked psychological stress with premature cellular aging as indexed by reduced leukocyte telomere

47 lomeres are the central timing mechanism for cellular aging, but also demonstrates that such a mechan

48 stress leading to DNA damage and accelerated cellular aging could contribute to these phenotypes.

49 ed one potential mechanism linking stress to cellular aging, disease and mortality in humans: telomer

50 the sine qua non of Gompertzian mortality is cellular aging, expressed through these two mitotic phen

51 ecision making, particularly impatience, and cellular aging, for the first time to our knowledge.

52 Reduced telomere length, as a proxy for cellular aging, has been associated with numerous chroni

53 ere length (LTL) is a potential indicator of cellular aging; however, its relation to physical activi

54 and key roles for hTERT have been implied in cellular aging, immortalization, and transformation.

55 Changes associated with cellular aging in chronic infections could contribute to

56 epigenetic regulation, stress responses, and cellular aging in eukaryotic cells.

57 itigate the negative effect of impatience on cellular aging in females.

58 Markers of oxidative stress and cellular aging in reproductive tract tissues were assess

59 Cellular aging in Saccharomyces cerevisiae is accompanie

60 ultures of three cardinal characteristics of cellular aging in vivo recommends it as a model for agin

61 oxidative stress; and (e) a milieu of muscle cellular aging in which these changes occur.

62 en receptor polymorphisms temper accelerated cellular aging in young females who tend to make impatie

63 ) and telomerase activity, two biomarkers of cellular aging, in a sample of postmenopausal women at r

64 leukocyte telomere length (LTL), a marker of cellular aging, in HIV-infected and uninfected adults.

65 Alterations in cellular aging, indexed by leukocyte telomere length (LT

66 These studies indicate that cellular aging is a critical determinant of primary-cell

67 Cellular aging is accompanied by alterations in gene exp

68 The effect of cellular aging is also studied through our model.

69 e in tissue death, providing evidence on how cellular aging is connected to its higher systemic conse

70 ular changes occurring during the process of cellular aging is crucial towards understanding the unde

71 Cellular aging is largely attributable to damage to DNA

72 To determine whether cellular aging leads to a cardiomyopathy and heart failu

73 n cynical hostility and two known markers of cellular aging, leukocyte telomere length (TL) and leuko

74 person associations between CES-D scores and cellular aging markers.

75 estigated the impact of environmental-driven cellular aging on wound healing by conducting a comprehe

76 Cellular aging plays an important role in many diseases,

77 linking long-term protein persistence to the cellular aging process.

78 r drugs and an advanced understanding of the cellular aging process.

79 ut whether the apoptosis results from normal cellular aging processes or accelerated cell loss upon g

80 e of gonadal hormones in women combined with cellular aging processes promote sex biases in stress dy

81 Cellular aging programs typically rely on the asymmetric

82 e regions as candidate genes with fertility, cellular aging, stress resistance and male-specific effe

83 , cells die without the classic hallmarks of cellular aging, such as progressive changes in size, dou

84 ic stem cells to DNA double-strand breaks to cellular aging, suggesting DNA integrity influences stem

85 ated relationships between vitamin D status, cellular aging (telomere length) and anti-telomere antib

86 Senescence is a form of cellular aging that limits the proliferative capacity of

87 se findings suggest a conserved mechanism of cellular aging that may be related to nucleolar structur

88 This accelerated cellular aging was associated with a declined ovarian re

89 the decade since the telomere hypothesis of cellular aging was proposed, the two essential genes for

90 Telomere length (TL) is a marker of cellular aging, with the majority of lifetime attrition