ライフサイエンスコーパス: aging-related

1 We predict such genes to be aging-related.

2 show that TP53INP1 deletion has no impact on aging-related accumulation of HSCs.

3 expression reversals may be associated with aging-related accumulation of stochastic effects that le

4 dipocytes is a hallmark of adipose aging and aging-related adipose dysfunction.

5 uring ER stress and indicate that genetic or aging-related alterations in PERK signaling can exacerba

6 s of SIRT2 reduces AMPK activation, promotes aging-related and Ang II-induced cardiac hypertrophy, an

7 e aimed to investigate the roles of SIRT2 in aging-related and angiotensin II (Ang II)-induced pathol

8 In contrast, human OA and aging-related and surgically induced OA in mice are asso

9 ar cartilage and in knee joints of mice with aging-related and surgically induced OA, using immunohis

10 Klotho may play a role in preventing aging-related arteriolar hyalinosis.

11 e TNF receptor-1 gene (TNFR1) contributes to aging-related atherosclerosis in humans and whether Tnfr

12 mans and whether Tnfr1 expression aggravates aging-related atherosclerosis in mice.

13 of the basal forebrain, which later develop aging-related atrophy and degenerative changes, as in AD

14 Elevated rate of aging-related biological and functional decline, termed

15 s rather than enhance the expression of skin aging-related biomarkers ex vivo.

16 review summarizes available observations of aging-related biomass burning aerosol mass concentration

17 Aging-related bone loss and osteoporosis affect millions

18 urons is an attractive approach for modeling aging-related brain disorders.

19 ntracellular Ca(2+) responses, reverses both aging-related Ca(2+) dysregulation and cognitive impairm

20 g FKBP1b is a molecular mechanism underlying aging-related Ca2+ dysregulation and unhealthy brain agi

21 lude that TNFR1 polymorphisms associate with aging-related CAD in humans, and TNFR1 contributes to ag

22 In tissues susceptible to aging-related cancers, including the prostate, a relaxat

23 diates canonical Wnt signaling, for roles in aging-related cardiac dysfunction.

24 mice were subjected to the investigation of aging-related cardiac hypertrophy.

25 ves play key roles in cardiac physiology and aging-related cardiovascular diseases.

26 e (NTPPPH) activity are strongly linked with aging-related cartilage calcification in meniscal and ar

27 signaling interaction is a new mechanism in aging-related cartilage pathology.

28 Mechanisms leading to the aging-related cartilage surface degeneration remain to b

29 Aging-related cellular and molecular processes including

30 on the efficacy of glucosamine in modifying aging-related cellular changes and supporting joint heal

31 Aging-related centromeric cohesion loss underlies premat

32 Nox2 activation is an important mechanism in aging-related cerebral capillary rarefaction and reduced

33 better understanding the molecular basis of aging related changes in neuroendocrine stress systems.

34 nces in the incidence of hypertension and in aging-related changes in blood pressure by neighborhood

35 However, longitudinal aging-related changes in brain functional modular archit

36 stic of aging human brain, and may influence aging-related changes in brain functions.

37 ued progress is being made on characterizing aging-related changes in cartilage.

38 us, this study reveals a novel mechanism for aging-related changes in CD8 T cells.

39 CR attenuated aging-related changes in cell type composition, gene exp

40 In sum, we have identified aging-related changes in cTfh that correlated with reduc

41 We examined age- and aging-related changes in functional architecture of the

42 current studies were performed to determine aging-related changes in polymorphonuclear neutrophil (P

43 ed single-cell RNA-sequencing to interrogate aging-related changes in the HFSCs.

44 These results support the concept that aging-related changes in the prostate microenvironment m

45 ort the identification of genes that exhibit aging-related changes of mRNA levels.

46 Although few significant aging-related changes were observed, robust sex differen

47 However, these aging-related changes were reduced or absent in Nox2 kno

48 ss questions concerning genetic influence on aging-related characteristics.

49 go a transition to beta-sheet as a result of aging-related chemical modifications of aspartyl residue

50 tress, has increased activity with aging and aging-related chronic diseases.

51 Aging-related chronic inflammation is a risk factor for

52 l cortex, an area previously associated with aging-related cognitive changes, is critical for normal

53 E (apoE) is a strong genetic risk factor for aging-related cognitive decline as well as late-onset Al

54 n changes in white matter microstructure and aging-related cognitive decline during the eighth decade

55 Aging-related cognitive decline is a primary risk factor

56 Aging-related cognitive decline is an emerging health cr

57 One contributor to aging-related cognitive decline is decreased intrinsic e

58 Understanding aging-related cognitive decline is of growing importance

59 ociated with pathological features of AD and aging-related cognitive decline.

60 iation in the human structural connectome in aging-related cognitive decline.

61 lar organization and their associations with aging-related cognitive decline.

62 Aging-related cognitive declines are well documented in

63 e that a reduction in neurogenesis underlies aging-related cognitive deficits and impairments in diso

64 w way to fight mild cognitive impairment and aging-related cognitive deterioration.

65 and increased glial activation, resulting in aging-related cognitive dysfunction.

66 nflammation in glia that cumulatively induce aging-related cognitive impairment.

67 f health-promoting substances by adults with aging-related cognitive or physical disorders.

68 ty associated with IIM may be complicated by aging-related comorbidities and decreased physical activ

69 Aging-related comorbidities are more common in people wi

70 onally, improved survival is associated with aging-related comorbidities such as diabetes and cardiov

71 Shortened LTL is observed in a host of aging-related complex genetic diseases and is associated

72 c disorders as well as neurodegenerative and aging-related conditions that are associated with loss o

73 e hubs integrating information from multiple aging-related conduits, including a peroxiredoxin-depend

74 In contrast, the aging-related contraction of the lymphoid compartment is

75 rominent with advancing age, suggesting that aging-related cortical demyelination contributes to incr

76 ange rates and extrapolated to further adult aging-related cortical thinning.

77 tive effect of GR levels associated with the aging-related cumulative characteristics of periodontal

78 s, presumably by slowing the accumulation of aging-related damage.

79 nd those that are enriched in 'ground truth' aging-related data; (iii) providing evidence that diseas

80 Center, moderate CR lowered the incidence of aging-related deaths.

81 treatment (acute vs chronic) and whether the aging-related decline in a particular cognitive process

82 ver, the molecular mechanisms underlying the aging-related decline in cardiac muscle function are lar

83 umans as well as other mammals experience an aging-related decline in drug metabolism as well as a di

84 Smoking may accelerate the aging-related decline in glomerular filtration rate.

85 eletal muscles, and a protection against the aging-related decline in nicotinate and nicotinamide met

86 fractional anisotropy (FA) as a biomarker of aging-related decline in white matter (WM) integrity to

87 8 years were composited to form a measure of aging-related decline, termed Pace-of-Aging.

88 uggesting that TRAP exposures may accelerate aging-related declines in health.

89 eritable diseases, acquired pathologies, and aging-related declines in health.

90 found that patients with SLE exhibit unique aging-related decreases in IFN signaling that correlate

91 Aging-related decreases in nitric oxide production have

92 tests of motor coordination, and both showed aging-related decreases in the size of the dopaminergic

93 hogen-derived products, had little effect on aging-related defects in NK cell priming.

94 ding DNA damage, is thought to contribute to aging-related degenerative changes, but how damage drive

95 ogy of aging, as well as the pathogenesis of aging-related degenerative diseases.

96 ss and telomere shortening/dysfunction cause aging-related degenerative pathologies and increase canc

97 Cerebral myelin maturation and aging-related degradation constitute fundamental feature

98 increase in survival, an attenuation of the aging-related deterioration of skeletal muscles, and a p

99 cyte telomere length (LTL) is a predictor of aging-related disease and decreases with each cell cycle

100 Osteoporosis is a common aging-related disease diagnosed primarily using bone min

101 this repair mechanism very likely increases aging-related disease susceptibility.

102 changes contribute to the increased risk of aging-related disease, such as cancer, are incompletely

103 ecific stem cells in homeostasis, aging, and aging-related disease.

104 as an attractive therapeutic target for many aging related diseases, however, how its activity can on

105 enous sources, creating lesions that lead to aging related diseases, including cancer.

106 ng because its shortening is associated with aging-related diseases and early mortality.

107 pro-inflammatory cytokines, contributing to aging-related diseases and morbidity.

108 n, delay, and/or alleviation of a variety of aging-related diseases and sequelae.

109 a new therapeutic approach for obesity- and aging-related diseases associated with mitochondrial dys

110 e that promotes mitochondrial dysfunction in aging-related diseases by catalyzing pathological remode

111 t studies are identifying pathways for these aging-related diseases by examining how the process of a

112 ll telomere attrition predicts mortality and aging-related diseases in inherited telomere syndrome pa

113 egulation of this process has been linked to aging-related diseases such as type 2 diabetes.

114 ted with an increased risk of brain atrophy, aging-related diseases, and mortality.

115 t6 activation protects against metabolic and aging-related diseases, and Sirt6 inhibition is consider

116 ith accelerated aging and increased risk for aging-related diseases, but the underlying molecular mec

117 se risks of cardiovascular disease and other aging-related diseases, but their relationships with leu

118 l inhibitors of SIRT2, an enzyme involved in aging-related diseases, e.g., neurodegenerative disorder

119 omere shortening has been linked to multiple aging-related diseases, including cancer.

120 prevent telomere-associated diseases, namely aging-related diseases, including cancer.

121 ulated genes showed enriched association for aging-related diseases, including coronary artery diseas

122 Because TL plays a significant role in aging-related diseases, insight into the factors that fa

123 ibution of CHIP to myriad cardiovascular and aging-related diseases, the epidemiology and biology sur

124 ated pathways involved in the development of aging-related diseases.

125 etic tools for studying vertebrate aging and aging-related diseases.

126 induction and perpetuation of metabolic and aging-related diseases.

127 stress, abnormalities of which underlie many aging-related diseases.

128 s have beneficial effects in metabolism- and aging-related diseases.

129 process, decrease during normal aging and in aging-related diseases.

130 promising strategy to prevent and alleviate aging-related diseases.

131 s a hallmark of aging and has been linked to aging-related diseases.

132 g genes associated with human autoimmune and aging-related diseases.

133 umulation, and aggregation characterize many aging-related diseases.

134 nd that LTL is relatively short in a host of aging-related diseases.

135 ell exhaustion in DC, PF, and possibly other aging-related diseases.

136 activity correlates with the development of aging-related diseases.

137 mechanism but also contributes to aging and aging-related diseases.

138 and stress responses, and are implicated in aging-related diseases.

139 rotein in cells is associated with aging and aging-related diseases; however, the roles of insoluble

140 s for progress in molecular understanding of aging-related disorders and neurodegenerative diseases.

141 ociated with increased life span and reduced aging-related disorders and reduces fibrosis in several

142 logy in humans and may provide insights into aging-related disorders linked to altered LTL dynamics.

143 ution (DPD) can slow the progression of some aging-related disorders, whether this strategy affects t

144 therapeutic strategies to delay the onset of aging-related disorders.

145 new therapeutic target for alleviating human aging-related disorders.

146 n joint disease and typically begins with an aging-related disruption of the articular cartilage surf

147 A GA should include high priority aging-related domains known to be associated with outcom

148 molecular evolution rates and predicting new aging-related drugs based on drug-gene interaction data.

149 The dichotomy of learning-related and aging-related effects on two very similar calcium-depend

150 Gpx1 Tg mice were protected from this aging-related enhanced susceptibility to venous thrombos

151 rded in total (1 AIDS event, 65 SNAEs and 96 aging-related events).A positive EAA by Horvath's clock

152 ock was associated with a 50% higher risk of aging-related events.

153 far, many microarray studies have addressed aging-related expression patterns in multiple organisms

154 The combination of 2 aging-related factors (ie, decline in both the mass and

155 here has been steady progress in identifying aging-related factors such as reactive oxygen species an

156 s study, we describe a strategy for inducing aging-related features in human iPSC-derived lineages an

157 re-related FEV(1) decrement equaled 12 yr of aging-related FEV(1) decline.

158 tial of fruits and vegetables may ameliorate aging-related frailty.

159 Aging-related functional impairments may inform risk pre

160 Aging-related functional NK cell deficiency is well docu

161 Finally, we found that aging-related functional NK cell deficiency was complete

162 the aged host environment is responsible for aging-related functional NK cell deficiency.

163 tor agonists may be useful tools in treating aging-related functional NK cell deficiency.

164 MicroRNAs (miRNAs) control aging-related functions such as metabolism and lifespan

165 Moreover, the idea of aging-related gains in wisdom is consistent with views o

166 Because the mRNA level of the senescence (aging)-related gene was significantly elevated in sample

167 Additionally, older mice exhibit more aging-related gene alterations in loops of Henle, proxim

168 sights, we integrate current static BNs with aging-related gene expression data to construct dynamic

169 Genes that changed with aging [aging-related genes (ARGs)] were identified in each regi

170 ng significant overlap between our predicted aging-related genes and 'ground truth' aging-related gen

171 o-longevity genes, revealing new insights on aging-related genes as a whole and their interactions wi

172 First, by classifying aging-related genes as pro- or anti-longevity, we define

173 tified 24 novel but well-supported candidate aging-related genes for further experimental validation.

174 ive set of network characteristics for human aging-related genes from the GenAge database.

175 Although some individual aging-related genes have been the subject of intense scr

176 of aging and the effects of perturbing known aging-related genes on lifespan and behavior.

177 ated diseases are due to a small fraction of aging-related genes which also tend to have a high netwo

178 Our subsequent comparison of aging-related genes with age-related disease genes revea

179 We provide comprehensive datasets of aging-related genes, pathways and ligand-receptor intera

180 multi-omics data, comprehensively annotating aging-related genes, proteins, metabolites, mitochondria

181 he gerontome across species, including human aging-related genes.

182 icted aging-related genes and 'ground truth' aging-related genes; (ii) observing significant overlap

183 er adults who are potentially susceptible to aging-related health conditions; however, the manifestat

184 Considering the aging-related health risks that the centenarians have su

185 ng hypotheses about causes and treatment for aging-related hepatic changes.

186 mics and functional significance of putative aging-related heterogeneity are also unknown.

187 ein we performed a biophysical separation of aging-related high molecular weight aggregates, isolated

188 e hypothesis that declining FKBP1b underlies aging-related hippocampal Ca2+ dysregulation.

189 ons have been postulated to account for many aging-related immune dysfunctions.

190 rts the hypothesis that the primary cause of aging-related impairment of muscle function is a cumulat

191 elevated levels of superoxide contribute to aging-related impairments in hippocampal LTP and memory,

192 Aging-related impairments in hippocampus-dependent cogni

193 An aging-related increase was found in high-threshold Ca an

194 rat hippocampal slice CA1 neurons have found aging-related increases in long-lasting calcium (Ca)-dep

195 40% caloric restriction (CR) did not exhibit aging-related increases in oocyte aneuploidy, chromosoma

196 Aging-related increases in systolic blood pressure were

197 ing in both age groups, only the sAHP showed aging-related increases.

198 (iNOS) expression, which are associated with aging-related inflammation and insulin resistance.

199 nuclear and cytosolic sirtuin inhibition to aging-related inflammatory disease development.

200 Accumulating evidence indicates that aging-related inflammatory responses are mechanistically

201 rget of cellular stress, toxin exposure, and aging-related injury.

202 ring islet regeneration, is depressed during aging-related islet dysfunction, and may be important in

203 Osteoarthritis (OA), the most prevalent aging-related joint disease, is characterized by insuffi

204 ent firing capacity, which may contribute to aging-related learning impairments.

205 fic calpain inhibition would protect against aging-related lesions in arteries and kidneys.

206 itical need for rapid model systems to study aging-related liver changes.

207 by memory CD8(+) T cells, which exhibited an aging-related loss in binding of NF-kappaB and STAT fact

208 SIRT1 agonist can restore this aging-related loss of cardioprotection.

209 clinical significance of Nox2-derived ROS in aging-related loss of cerebral capillaries and neurons w

210 In human and murine cartilage, there is an aging-related loss of HMGB2 expression, ultimately leadi

211 To understand if this results in aging-related loss of immune protection against emerging

212 es muscle size and growth rate, accelerating aging-related loss of muscle mass and function.

213 In OA they display aging-related loss of proliferation but no gross osteoge

214 ot restricted to IPF and also occur in other aging-related lung disorders, primarily chronic obstruct

215 ent decreased accumulation of lipofuscin, an aging-related marker, in the brain and enhanced proteaso

216 ved fibroblasts and neurons induces multiple aging-related markers and characteristics, including dop

217 To gain insight into aging-related mechanisms in ALI, we investigated the eff

218 Targeting aging-related mechanisms is a potential therapeutic stra

219 Aging-related Meibomian gland shrinkage may result in pa

220 An aging-related microbiome score, generated via combinatio

221 An aging-related miRNA, miR-29b-5p, was first found to be m

222 ated mice showed up-regulation of a panel of aging-related miRs.

223 the aging brain, and provide a link between aging-related molecular changes and functional decline.

224 However, evaluations of aging-related mtDNA mutations in other model animal syst

225 n young adult mice, and remarkably, prevents aging-related muscle changes in old adult mice, resultin

226 RET may have a stronger effect in preventing aging-related muscle mass attenuation and leg strength l

227 and the molecular mechanisms underlying this aging-related network specificity, we also analyzed prot

228 ctly associated with conditions of aging and aging-related neurodegeneration.

229 Oxidative stress plays an important role in aging-related neurodegeneration.

230 oth the aging process and the development of aging-related neurodegenerative brain diseases.

231 onic microinflammation is a hallmark of many aging-related neurodegenerative diseases as well as meta

232 ylated tau, are a common feature of numerous aging-related neurodegenerative diseases, including Alzh

233 ways also modulate fundamental mechanisms in aging-related neurodegenerative diseases, including prot

234 or factor contributing to the development of aging-related neurodegenerative diseases, notably Alzhei

235 uleus (LC) neurons is a prominent feature of aging-related neurodegenerative diseases, such as Parkin

236 evelopment of a therapeutic approach against aging-related neurodegenerative disorders such as Alzhei

237 tion has been identified as a contributor to aging-related neurodegenerative disorders such as Alzhei

238 heimer disease (AD), the most common form of aging-related neurodegenerative disorders, is associated

239 is also a pathological feature of the major aging-related neurodegenerative disorders.

240 ficient ((-/-)) female mice would have lower aging-related neuroinflammation than wild type (WT).

241 tly affect fatty acid metabolism and augment aging-related neuroinflammation.

242 g p75(NTR) function would prevent or reverse aging-related neuronal degeneration using LM11A-31, a sm

243 mechanism for therapeutic intervention into aging-related neuronal disorders.

244 We argue that reversals may not represent aging-related neuronal loss.

245 an important component in the development of aging-related non-melanoma skin cancer.

246 Aging-related organ degeneration is driven by multiple f

247 e differences in prevalence and incidence of aging-related outcomes in a rural population (1,358 comm

248 irs the ability of the RPE to defend against aging-related oxidative stress.

249 intake on telomere length and other cellular aging-related parameters of glucose and insulin metaboli

250 ssfully demonstrated to mitigate a myriad of aging-related pathologies and to cull senescent cancer c

251 which represents a viable option to address aging-related pathologies in diabetes and neurodegenerat

252 ent of autophagy may protect against certain aging-related pathologies such as OA.

253 e and genotoxic stresses, protection against aging-related pathologies, and promotion of metabolic ho

254 Aging related phenomena of ooplasmic microtubule dynamic

255 The mechanism behind this aging-related phenomenon is unknown and has been difficu

256 n of Pofut1 in skeletal myofibers can induce aging-related phenotypes in cis within skeletal myofiber

257 t al. (2013) provide a strategy for inducing aging-related phenotypes in hiPSC-derived neurons, enabl

258 1 inhibitor, strikingly ameliorated multiple aging-related phenotypes.

259 The most important aging-related phenotypic effects observed were those tha

260 Biological age measurements (BAs) assess aging-related physiological change and predict health ri

261 ng may uncover novel therapeutic targets for aging-related physiologies.

262 n regulating mammalian genomic stability and aging-related physiology.

263 ctions and diseases that are enriched in our aging-related predictions and those that are enriched in

264 ence that diseases which are enriched in our aging-related predictions are linked to human aging; and

265 rcc1-deficient liver differs from the normal aging-related process.

266 sting that abscisic acid is involved in root aging-related processes characterized by expression chan

267 Aging-related processes in plant tissues are associated

268 This temporal sequence of aging-related processes in roots is highly reminiscent o

269 Aging-related processes involve changes in the expressio

270 eneration by altering the homeostasis of key aging-related processes.

271 ially in diseases of human aging and in some aging-related processes.

272 may indicate a physiological role for NO in aging-related processes.

273 nce of noncancer cfDNA mutants attributed to aging-related processes.

274 of reactive oxygen species (ROS) and delays aging-related processes.

275 oteasome inhibition within neurons, to mimic aging-related reduction of proteasome activity, induced

276 In the present study, the effects of AG on aging-related renal and vascular changes and AGE accumul

277 ng the renal vasculature and contributing to aging-related renal function decline.

278 suggest that PPAR-gamma agonists may benefit aging-related renal injury by improving mitochondrial fu

279 noncoding RNAs (ncRNA) also associated with aging-related senescence and cancer, but whether ncRNAs

280 asthma, cancer, neurological disorders, and aging-related sequelae.

281 These results show that iNs retain important aging-related signatures, thus allowing modeling of the

282 urce of cell-free product for attenuation of aging-related skin and vascular dysfunctions due to thei

283 ermal dysfunction and skin damage as well as aging-related skin diseases, such as epidermal thinning

284 or developing therapeutic strategies against aging-related skin disorders.

285 sorder (MDD) have an increased onset risk of aging-related somatic diseases such as heart disease, di

286 tudinal studies, convincing evidence for the aging-related somatic expansion of the C150T mutation, u

287 We propose that AD is initiated by a protein aging-related structural transformation in soluble Abeta

288 Moreover, aging-related superiority in perceiving background motio

289 r predisposition, atherosclerosis, and other aging related symptoms.

290 isplays multiple phenotypes resembling human aging-related syndromes.

291 ognize and manage multiple comorbidities and aging-related syndromes.

292 thogenic in a manner distinct from classical aging-related tauopathy, underlining the importance of a

293 The association between aging-related testosterone deficiency and late-onset hyp

294 imilarities of this phenotype to accelerated aging-related thymic involution support the possibility

295 A shift in sphingolipid patterns during aging related to myelin remodeling is accompanied by lar

296 dementia, albeit with increased, presumably aging-related variability, and identify sets of co-expre

297 blast cells and contained a large number of aging-related variants.

298 Aging-related vascular and cardiac deposition of Alphabe

299 otype shift to "reactive" ependymal cells in aging-related ventricle stenosis; moreover, they also co

300 baseline total activity score minimized this aging-related weight loss, but this relation was most pr