ライフサイエンスコーパス: cellular aging

1 d PTSD have been associated with accelerated cellular aging.

2 Oxidative damage plays a central role in cellular aging.

3 e our understanding of growth regulation and cellular aging.

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

5 omarkers that more closely index the rate of cellular aging.

6 ion for counterintuitive race differences in cellular aging.

7 1) activity that, subsequently, accelerates cellular aging.

8 f1 to maintain autophagy and survival during cellular aging.

9 ondrial metabolic activity, two hallmarks of cellular aging.

10 cal pathways related to oxidative stress and cellular aging.

11 nes, inflammation, immune cell function, and cellular aging.

12 are particularly vulnerable and adaptable to cellular aging.

13 or cellular senescence, is a major factor in cellular aging.

14 maintaining redox homeostasis and preventing cellular aging.

15 d suggest CME as a potential driver of early cellular aging.

16 ng a classical biological model for studying cellular aging.

17 hways demonstrated altered activation during cellular aging.

18 chromosomes, and their length is a marker of cellular aging.

19 chondrial structure that is activated during cellular aging.

20 may also slow the process of senescence, or cellular aging.

21 ormed our understanding of the mechanisms of cellular aging.

22 a on inflammaging and molecular processes of cellular aging.

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

24 ality partly via accelerating the process of cellular aging.

25 of mitochondrial biogenesis are involved in cellular aging.

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

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

28 e are conserved processes that contribute to cellular aging.

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

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

31 mulation of mitochondria occurs often during cellular aging.

32 n maintaining telomere length and preventing cellular aging.

33 ans, and have implications for understanding cellular aging.

34 t hostility might impact health by promoting cellular aging.

35 ogens may be associated with deceleration of cellular aging.

36 These effects may be mediated by accelerated cellular aging.

37 Protein damage contributes prominently to cellular aging.

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

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

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

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

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

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

44 of cancer progression, stem cell renewal and cellular aging(2-5).

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

46 Cellular aging, a progressive functional decline driven

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

48 required to assess the long-term effects of cellular aging after SVR.

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

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

51 ainly caused by oxidative stress, leading to cellular aging and breakdown of the extracellular matrix

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

53 hand, defects in physiologic regulations of cellular aging and death (escape from cellular senescenc

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

55 d products (AGEs) on biopolymers accompanies cellular aging and drives poorly understood disease proc

56 ic landscape organization and its changes in cellular aging and for identifying aging drivers and int

57 ntelligence (AI) models to assess individual cellular aging and found that many eye diseases not asso

58 leukocyte telomere length (LTL), a marker of cellular aging and genomic instability, in the associati

59 e shortening is a well-established marker of cellular aging and genomic instability.

60 sustained ion release over 28 days, reducing cellular aging and inflammation in nucleus pulposus cell

61 We also consider the roles of cellular aging and intrinsic and extrinsic stimuli in mo

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

63 ll-omics" strategy enhances comprehension of cellular aging and lays the groundwork for exploring the

64 (cluster of differentiation 38) in promoting cellular aging and lung fibrosis.

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

66 unwanted proteins contributes prominently to cellular aging and neurodegeneration.

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

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

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

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

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

72 Moreover, these data implicate cellular aging and senescence as a process that contribu

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

74 resistance to a variety of stressors, delays cellular aging and senescence.

75 te exchange interactions as a determinant of cellular aging and show that metabolically cooperating c

76 vision have been associated with accelerated cellular aging and the development of both cancer and ne

77 Cellular aging and the development of replicative senesc

78 ergoing structural-functional changes during cellular aging and their contributions to age-related ph

79 tailing molecular mechanisms associated with cellular aging and their implications for oral tissue he

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

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

82 In RA, T cells have several hallmarks of cellular aging, and they accumulate DNA damage, predispo

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

84 lecular-scale insights into the mechanism of cellular aging are inferred.

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

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

87 further evidence for the characterization of cellular aging as a general process, affecting prokaryot

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

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

90 This study indicates that cellular aging can reveal late-onset disease phenotypes,

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

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

93 therapeutic intervention to slow the pace of cellular aging, disease onset, and neuropathology, parti

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

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

96 est that although hibernation may ameliorate cellular aging, foraging on human food subsidies could c

97 e investigated the association of individual cellular aging hallmarks with PD but not jointly.

98 ear, increased oxidative stress accelerating cellular aging has been shown to play a role.

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

100 genetic clocks, reflecting various facets of cellular aging, health, and mortality risk.

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

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

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

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

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

106 premier antioxidant that combats ROS-induced cellular aging in human skins.

107 However, whether p53-related cellular aging in mature white adipocytes is causative o

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

109 Cellular aging in Saccharomyces cerevisiae is accompanie

110 Am in PRC2 LMRs, as a universal biomarker of cellular aging in somatic cells which can distinguish th

111 gum disease may be a mechanism accelerating cellular aging in the gum tissue.

112 senescence has become a prominent model for cellular aging in vitro.

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

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

115 ignal polarization, could be weakened due to cellular aging in yeast and other cell types, leading to

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

117 ods influences hibernation, and subsequently cellular aging, in a large-bodied hibernator, black bear

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

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

120 nal capacity is associated with hallmarks of cellular aging, including decreased metabolic function a

121 , promotes a rapid and broad amelioration of cellular aging, including resetting of epigenetic clock,

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

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

124 Cellular aging is a multifactorial process that is chara

125 Cellular aging is accompanied by alterations in gene exp

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

127 Cellular aging is characterized by disruption of the nuc

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

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

130 age at a cellular level, demonstrating that cellular aging is inevitable.

131 description of the phenotypic changes during cellular aging is key towards unraveling its causal forc

132 Cellular aging is largely attributable to damage to DNA

133 lerated telomere shortening, an indicator of cellular aging, is a potential mechanism through which p

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

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

136 Cellular aging markers during Parkinson's disease (PD) h

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

138 Thus, increased cellular aging may be responsible for the absence of liv

139 alyze whether the parameters associated with cellular aging measured at the DAA initiation date are r

140 Telomere shortening is a well-characterized cellular aging mechanism, and short telomere syndromes c

141 siae (a powerful model organism to study the cellular aging of humans) and those with expression chan

142 e of importance for skin tumor formation and cellular aging of keratinocytes.

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

144 Cellular aging, particularly in adult stem cells, offers

145 y to poor health outcomes suggest a role for cellular aging pathways, casting obesity as a disease of

146 Cellular aging plays an important role in many diseases,

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

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

149 Understanding the mechanisms of the cellular aging processes is crucial for attempting to ex

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

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

152 1 (TOMITO) signaling process) that regulates cellular aging processes.

153 Cellular aging programs typically rely on the asymmetric

154 ned the impact of omega-3 supplementation on cellular aging-related biomarkers following a laboratory

155 istachio intake on telomere length and other cellular aging-related parameters of glucose and insulin

156 w added sugar consumption may support slower cellular aging relative to chronological age, although l

157 lidation identified new proteins involved in cellular aging, showing that these predictions and pheno

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

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

160 measured several parameters associated with cellular aging, such as telomere attrition, mitochondria

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

162 ed production of COL3, which was impaired by cellular aging, suggesting novel strategies to restore t

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

164 kocyte telomere length (LTL), a biomarker of cellular aging, than non-Hispanic White Americans.

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

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

167 f protein aggregation during heat stress and cellular aging, using Saccharomyces cerevisiae as a mode

168 Its overexpression accelerates cellular aging via mitochondrial dysfunction.

169 ross adolescence; and quantified the pace of cellular aging via telomere erosion across the second de

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

171 based actin turnover analysis to distinguish cellular aging was explored.

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

173 ulation, accumulation of cellular damage and cellular aging, which collectively contribute to the CdL

174 -targeting small molecule rescued markers of cellular aging, which establishes mitochondrial quality

175 Uncovering the regulators of cellular aging will unravel the complexity of aging biol

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