ライフサイエンスコーパス: senescent

1 pair the break, undergo apoptosis, or become senescent.

2 y exposed to chemotherapy but had never been senescent.

3 ve a lifespan of 120 days before they become senescent and again come into contact with macrophages.

4 ng their life cycle and thus require to shed senescent and damaged organs.

5 We conclude that high proportions of senescent and exhausted VZV-specific T cells in the olde

6 tal knee replacement decreased expression of senescent and inflammatory markers while also increasing

7 OCPCs and AhCPCs to overexpress NS decreases senescent and multinucleated cells, restores morphology,

8 expression and functional analyses comparing senescent and non-senescent B-cell lymphomas from Emu-My

9 on between improperly retained dysfunctional/senescent and normal mitochondria.

10 ls, by augmenting Notch signaling, provoke a senescent and pro-inflammatory state in endothelial cell

11 We found that PCI can distinguish between senescent and quiescent cells, which is extremely diffic

12 Inflated cells were polyfunctional, not senescent, and displayed high ex vivo levels of granzyme

13 Arrested tetraploid cells finally become senescent, as determined by SA-beta-galactosidase activi

14 NA sequencing revealed that a vast number of senescent-associated changes are dependent on mitochondr

15 of inflammatory genes that contribute to the senescent-associated secretory phenotype (SASP), and ove

16 ctional analyses comparing senescent and non-senescent B-cell lymphomas from Emu-Myc transgenic mice

17 m human adults contain p16(Ink4a)-expressing senescent beta cells and that senescence induced by p16(

18 ged mice effectively depleted SCs, including senescent bone marrow hematopoietic stem cells (HSCs) an

19 , and significant restoration of replicative senescent bone marrow mesenchymal ST2 cells (passaged 30

20 isorders, but the mechanisms that render the senescent brain vulnerable to disease are unclear.

21 de restorative benefit by mitigating accrued senescent burden.

22 cell surface DPP4 preferentially sensitized senescent, but not dividing, fibroblasts to cytotoxicity

23 was selectively expressed on the surface of senescent, but not proliferating, human diploid fibrobla

24 dentified that in human fibroblasts rendered senescent by stress, replicative exhaustion, or oncogene

25 Thus, large, old trees do not act simply as senescent carbon reservoirs but actively fix large amoun

26 x I expression and most CD8(+) T-cells had a senescent CCR7-CD127(-)CD28(-)CD57(+) phenotype with poo

27 Senescent CD4(+) and CD8(+) T cells may have differentia

28 heart failure was associated with increased senescent CD4+ T cells, and reduced naive and effector a

29 aive B cells, reduction in PD-1(+)CD4(+) and senescent CD57(+)CD4(-) T cells, and decreases in elevat

30 hat early-intervention suicide-gene-mediated senescent cell ablation improves pulmonary function and

31 hypothesis that exercise prevents premature senescent cell accumulation and systemic metabolic dysfu

32 Senescent cell accumulation in aging tissues is linked t

33 t may become impaired with age and result in senescent cell accumulation.

34 JAK inhibitor suppressed senescent cell activin A production and blunted senescen

35 Increased senescent cell burden in various tissues is a major cont

36 ar," as opposed to chronologic, age and that senescent cell clearance may mitigate aging-associated p

37 phage as a critical player in this efficient senescent cell clearance mechanism.

38 , but that rapid and effective mechanisms of senescent cell clearance operate in normal and regenerat

39 rs are detectable within IPF lung tissue and senescent cell deletion rejuvenates pulmonary health in

40 owth hormone axis perturbations, can promote senescent cell formation.

41 anscriptome signatures to detect any type of senescent cell or to discriminate among diverse senescen

42 This is driven in part by depolarization of senescent cell plasma membrane, which leads to primary c

43 Senescent cell production occurs throughout life and pla

44 ndicating that persistent signaling supports senescent cell survival.

45 ith specific senescence-inducing stresses or senescent cell types and identify and validate genes tha

46 Here, we identify FOXO4 as a pivot in senescent cell viability.

47 escent cell activin A production and blunted senescent cell-mediated inhibition of adipogenesis.

48 In vitro studies demonstrated that senescent-cell conditioned medium impaired osteoblast mi

49 images compared with 1 +/- 0/10 images), or senescent cells (4% +/- 1% compared with 4% +/- 1%).

50 ssity of CD4+ T cells for immunoclearance of senescent cells (Figure 4A).

51 Senescent cells (SCs) accumulate with age and after geno

52 Senescent cells (SnCs) accumulate in many vertebrate tis

53 Senescent cells accumulate in fat with aging.

54 Senescent cells accumulate in various tissues and organs

55 senescence and immune-mediated clearance of senescent cells after intrahepatic injection of NRAS (Fi

56 ples showed an increase in the proportion of senescent cells after treatment with bevacizumab had lon

57 determining the diverse biological roles of senescent cells and developing specific drug targets.

58 ounding a hypoxic core of primarily non-stem senescent cells and diffuse, quiescent CSCs.

59 mic H4K16ac-decorated chromatin landscape in senescent cells and enforces tumor suppression.

60 w that exercise prevents the accumulation of senescent cells and the expression of the SASP while nul

61 Therefore, senescent cells and the SASP represent significant oppor

62 e consistent with a possible contribution of senescent cells and the SASP to age-related inflammation

63 Here, we review recent studies on how senescent cells and the senescence-associated secretory

64 Given that eliminating senescent cells and/or inhibiting their proinflammatory

65 As a consequence, Ras-induced senescent cells are hindered in their ability to recruit

66 Together, these results demonstrate that senescent cells are key drivers of atheroma formation an

67 ariable, and methods for clearly identifying senescent cells are lacking [10].

68 if the senescence program is bypassed or if senescent cells are not cleared.

69 When chronically present, senescent cells are thought to enhance the age-dependent

70 Senescent cells are thought to impair tissue function, a

71 Identifying how senescent cells avoid apoptosis allows for the prospecti

72 actor receptor I (TNFRI) from the surface of senescent cells by ectodomain shedding.

73 The elimination of senescent cells by suicide gene-meditated ablation of p1

74 e that humoral innate immunity may recognize senescent cells by the presence of membrane-bound MDA-vi

75 d recent evidence suggests that clearance of senescent cells can also improve health and lifespan.

76 ting the proliferation of damaged cells, but senescent cells can also promote cancer though the pro-i

77 Recent studies now show that targeting senescent cells can enhance the functions of stem/progen

78 cence-associated secretory phenotype (SASP), senescent cells can paradoxically promote carcinogenesis

79 Senescent cells contribute to age-related tissue degener

80 ncept that transient therapeutic delivery of senescent cells could be harnessed to drive tissue regen

81 served deficiencies in DNA repair factors in senescent cells could contribute to the genomic instabil

82 Consistent with this, removal of senescent cells delays the onset of cancer and prolongs

83 Eliminating ATRX in senescent cells destabilizes the senescence-associated h

84 Furthermore, the number of senescent cells does not increase upon repetitive amputa

85 lective expression of DPP4 on the surface of senescent cells enables their preferential elimination.

86 ss is a potential trigger of senescence, and senescent cells exhibit characteristic functional resist

87 Here, we show that nonproliferating senescent cells express and incorporate histone H3.3 and

88 t the genetic or pharmacological ablation of senescent cells extends life span and improves health sp

89 Clearing senescent cells from 18-month-old naturally-aged INK-ATT

90 We previously found genetic clearance of senescent cells from progeroid INK-ATTAC mice prevents l

91 When the senescent cells from which CM was derived had been treat

92 We found a higher burden of senescent cells in adipose tissue with aging.

93 Here we investigate a role for senescent cells in age-related bone loss through multipl

94 armacological targets for the elimination of senescent cells in age-related disease.

95 and pharmacological approaches to eliminate senescent cells in atherosclerosis-prone low-density lip

96 vely, these data establish a causal role for senescent cells in bone loss with aging, and demonstrate

97 Human and mouse skin accumulate senescent cells in both the epidermis and dermis during

98 -meditated ablation of p16(Ink4a)-expressing senescent cells in INK-ATTAC mice or by treatment with a

99 Frequencies of senescent cells in liver and intestinal crypts quantitat

100 ntial accumulation of telomere-dysfunctional senescent cells in nfkb1(-/-) tissues is blocked by anti

101 propose that effective immunosurveillance of senescent cells in salamanders supports their ability to

102 l autonomous and non-autonomous functions of senescent cells in the context of skin aging and wound h

103 nd the autocrine and paracrine properties of senescent cells in the contexts of aging and age-related

104 o generate inflammatory protein release from senescent cells in the lung.

105 o the identification and characterization of senescent cells in tissues and organs.

106 This model suggests that the abundance of senescent cells in vivo predicts "molecular," as opposed

107 hat reactivation of telomerase expression in senescent cells is an early event during cancer progress

108 Thus, therapeutic targeting of senescent cells is feasible under conditions where loss

109 mechanism, the accumulation of DNA damage in senescent cells is thought to cause genomic instability,

110 class of senolytic drugs.The accumulation of senescent cells is thought to contribute to the age-asso

111 premalignant cells, yet the accumulation of senescent cells is thought to drive age-related patholog

112 echanistically, we show that mitochondria in senescent cells lose the ability to metabolize fatty aci

113 drives hepatic steatosis and elimination of senescent cells may be a novel therapeutic strategy to r

114 lopment and function of acute versus chronic senescent cells may lead to new therapeutic strategies f

115 Senescent cells may play a role in type 2 diabetes patho

116 Senescent cells may promote tumour progression through t

117 Thus, senescent cells might be part of a pathogenic loop in di

118 Accumulation of senescent cells occurs during aging and is also seen in

119 ence suggest that indiscriminately targeting senescent cells or modulating their secretome for anti-a

120 Our study indicates targeting senescent cells or their products may alleviate age-rela

121 ss, activation of the INK-ATTAC caspase 8 in senescent cells or treatment with senolytics or the JAKi

122 Senescent cells participate in a variety of physiologica

123 In vivo, these previously senescent cells presented with a much higher tumour init

124 In advanced lesions, senescent cells promote features of plaque instability,

125 However, when transiently present, senescent cells promote optimal wound healing.

126 Here we show that the accumulation of senescent cells promotes hepatic fat accumulation and st

127 Whether and how senescent cells regulate IPF or if their removal may be

128 Probe AHGa is transformed into AH in senescent cells resulting in an enhanced fluorescent emi

129 However, while arrested, senescent cells secrete a variety of proteins collective

130 Senescent cells secrete cytokines and other factors of t

131 Senescent cells secrete various growth factors and cytok

132 olytic with the potential to kill persistent senescent cells that accumulate during standard chemothe

133 may remain high due to the long lifespan of senescent cells that are not cleared.

134 Furthermore, elimination of senescent cells through temporary TGFbeta inhibition lea

135 lly redistributing between proliferating and senescent cells to parallel changes in expression.

136 umulation may thus promote the signalling of senescent cells to the immune system, and it may contrib

137 Senescent cells undergo dramatic alterations to their ch

138 oduction of the proinflammatory secretome of senescent cells using a JAK inhibitor (JAKi).

139 allowed flow cytometry-mediated isolation of senescent cells using anti-DPP4 antibodies.

140 The beneficial effects of targeting senescent cells were due to lower bone resorption with e

141 Senescent cells were positive for platelet-derived growt

142 Within this validation, senescent cells were recognized with 93% sensitivity and

143 However, in senescent cells where PANDA sequesters transcription fac

144 Meanwhile, the steady accumulation of senescent cells with age also has adverse consequences.

145 y and tumor suppression, but accumulation of senescent cells with age contributes to the functional d

146 ch they affect the behavior and accretion of senescent cells within distinct tissues is not clear.

147 nducible caspase 8 expressed specifically in senescent cells) or pharmacological (i.e., 'senolytic' c

148 inflammatory cytokines is increased in these senescent cells, a manifestation of the senescence-assoc

149 ry mediators that demarcate the secretome of senescent cells, also referred to as the senescence-asso

150 ily GTPases Rac1 and Cdc42 were activated in senescent cells, and simvastatin reduced both activities

151 tory macrophages, crown-like structures, and senescent cells, as well as a 2-step pancreatic clamping

152 oliferating and senescent cells; however, in senescent cells, but not proliferating cells, H4K20me3 e

153 In senescent cells, but not proliferating cells, promoters

154 Advanced atherosclerotic lesions contain senescent cells, but the role of these cells in atheroge

155 In senescent cells, H4K20me3 is especially enriched at DNA

156 ance and consequences of naturally occurring senescent cells, here we use a previously established tr

157 cumulation of H4K20me3 at repressed genes in senescent cells, including at genes also repressed in pr

158 1, elevated in dividing cells and reduced in senescent cells, sequesters let-7 to enable a proliferat

159 genome of pre-malignant, oncogene-expressing senescent cells, thereby suppressing epigenetic and gene

160 In senescent cells, this selectively causes p53 nuclear exc

161 They also suggest that senescent cells, which accumulate after radio/chemo ther

162 for the preferential ligand upregulation on senescent cells, which are preferentially killed by NK c

163 brotic lung disease is mediated, in part, by senescent cells, which can be targeted to improve health

164 s (ECFCs) can be explained by the absence of senescent cells, which in mature endothelial cells occup

165 ., 'senolytic' compounds) means to eliminate senescent cells.

166 idly identify drugs that specifically affect senescent cells.

167 a differentiation program characteristic of senescent cells.

168 selective markers to monitor the presence of senescent cells.

169 rs in differentiating progenitors exposed to senescent cells.

170 tone variant H2A.Z at INK4 gene promoters in senescent cells.

171 or Cdc42 depletion reduced IL-6 secretion by senescent cells.

172 dify the cellular markers characteristic for senescent cells.

173 e in fully quiescent differentiated cells or senescent cells.

174 emotherapy-treated cancer cells enriched for senescent cells.

175 in gene expression between proliferating and senescent cells; however, in senescent cells, but not pr

176 r cell strains and between proliferating and senescent cells; however, in the four aging cell strains

177 To assess senescent changes in systemic immune response efficacy w

178 emonstrate that this hydroxylation occurs in senescent chloroplasts of Arabidopsis thaliana.

179 red a combined targeting strategy to deplete senescent cholangiocytes and ASFs from fibrotic tissue t

180 Persistent secretion of growth factors by senescent cholangiocytes leads to the activation of stro

181 Using a coculture system, we determined that senescent cholangiocytes promoted quiescent mesenchymal

182 ith A-1331852 resulted in an 80% decrease in senescent cholangiocytes, a reduction of fibrosis-induci

183 uced the survival and increased apoptosis of senescent cholangiocytes, compared to nonsenescent cells

184 y a dual effect on activated fibroblasts and senescent cholangiocytes.

185 Bcl-xL was also up-regulated in senescent cholangiocytes.

186 a key survival factor in ASFs as well as in senescent cholangiocytes.

187 Senescent chondrocytes are found in cartilage tissue iso

188 In an asymptomatic, senescent community-dwelling population, we observed a d

189 ow that simvastatin mitigates the effects of senescent conditioned media on breast cancer cell prolif

190 cholangiocytes and in experimentally induced senescent cultured cholangiocytes; inhibition of Ras abr

191 In contrast, older mothers demonstrate a senescent decline in pre-natal allocation but allocate m

192 ase in performance followed by a late - life senescent decline.

193 Senescent declines in reproduction and survival are foun

194 In the species exhibiting senescent declines, we also detected a terminal improvem

195 Because juvenile and senescent donor hepatocytes were likewise functional, ho

196 e oxygen species (ROS) also mediated the pro-senescent effect of RSV, it occurred after S-phase arres

197 However, the extent to which senescent elevations in infection mortality are causally

198 his study examined the potential of MPs from senescent endothelial cells (ECs) or from patients with

199 Interestingly, senescent endothelial cells do not mount a typical senes

200 terized by a proinflammatory, apoptotic, and senescent endothelial phenotype.

201 Splenic red pulp macrophages (RPM) degrade senescent erythrocytes and recycle heme-associated iron.

202 C1, also known as Ly-6C) ingest stressed and senescent erythrocytes, accumulate in the liver via coor

203 ort that increased IL10, not IL4 or IL13, in senescent eyes activates STAT3 signalling that induces t

204 Here we show that primary human senescent fat progenitors secrete activin A and directly

205 protein stress, enhancing the apoptotic and senescent fates.

206 We show that senescent fibroblasts and endothelial cells appear very

207 olin-1-specific cytokine that is secreted by senescent fibroblasts following the caveolin-1-mediated

208 The caveolin-1-mediated secretion of IL-6 by senescent fibroblasts stimulates the growth of cancer ce

209 Moreover, in replicative human senescent fibroblasts, DDR precluded MYOD-mediated activ

210 We show that the secretome of senescent fibroblasts, which are selectively killed by a

211 ty to activate the myogenic program in human senescent fibroblasts.

212 cular RNA showing markedly reduced levels in senescent fibroblasts.

213 However, senescent foliage falling from treated trees represents

214 g protein prenylation, without affecting the senescent growth arrest.

215 functionally competent CSCs persists in the senescent heart and that this stem cell compartment can

216 Thus, while senescent hepatocyte-secreted chemokines suppress liver

217 s termed "senescence surveillance." However, senescent hepatocytes give rise to hepatocellular carcin

218 term treatment with growth hormone augmented senescent host liver repopulation involving the growth h

219 functional, host-derived factor(s) impaired senescent host liver repopulation.

220 ared in juvenile, but only small clusters in senescent host livers.

221 istribution of H4K20me3 in proliferating and senescent human cells.

222 nstrated using early versus late passage and senescent human diploid fibroblasts, documenting the ant

223 show that simvastatin decreases the SASP of senescent human fibroblasts by inhibiting protein prenyl

224 Conditioned medium (CM) from senescent human preadipocytes induced macrophage migrati

225 Senescent human primary preadipocytes as well as human u

226 tion of the immune system are referred to as senescent immune remodeling (SIR).

227 IL that are characteristically exhausted and senescent is not established.

228 ar RNAs in proliferating (early-passage) and senescent (late-passage) human diploid WI-38 fibroblasts

229 (due to neonicotinoids' systemic nature) via senescent leaves.

230 translational start site in both, mature and senescent leaves.

231 HCC cell lines prevented the emergence of a senescent-like phenotype and induced synergistic global

232 erproliferation of melanocytes that are in a senescent-like state, but with occasional malignant tran

233 d PC cell growth and increased the number of senescent LNCaP cells.

234 Determination of senescent lymphocytes should be part of the diagnostic e

235 antly lower TRPM2 expression than those from senescent mice and had significantly lower viability aft

236 haracterized by the presence of reactive and senescent microglial cells in the frontal cortex.

237 roduce failures of turnover, accumulation of senescent mitochondria in the axon, defects in mitochond

238 t Parkin-deficient animals do not accumulate senescent mitochondria in their motor axons or neuromusc

239 y, which was associated with accumulation of senescent mitochondria.

240 of senescence, we immunized BALB/c mice with senescent mouse lung fibroblasts and screened for antibo

241 e marrow hematopoietic stem cells (HSCs) and senescent muscle stem cells (MuSCs).

242 repolarization and diastolic tension of the senescent myocardium are partly restored.

243 tion in peripheral tissues, and clearance of senescent neutrophils.

244 d prior to nodule formation and also in nifH senescent nodules.

245 including young nodules, mature nodules and senescent nodules.

246 ts maximum in mature nodules and decaying in senescent nodules.

247 ome analysis of actively dividing and deeply senescent normal human epithelial cells.

248 ty after silica NPs exposure than those from senescent ones.

249 Macrophages recognize and phagocytose senescent or damaged erythrocytes.

250 tional Parkin-mediated mitophagic culling of senescent or damaged mitochondria is a major pathologica

251 ophagy pathways to sequester macromolecules, senescent organelles, and pathogens.

252 ng bone mass and microarchitecture in SAMP-6 senescent osteopenic mice.

253 Exposure of P1 ECs to MPs shed from senescent P3 cells or circulating MPs from ACS patients

254 Ageing generates senescent pathologies, some of which cause death.

255 s, thereby facilitating the development of a senescent phenotype and CKD.

256 Furthermore, Sin3B is required for the senescent phenotype and elevated levels of reactive oxyg

257 oteinase 10 on MM cells is associated with a senescent phenotype and requires generation of reactive

258 usly, we showed that mitochondria-driven pre-senescent phenotype diminishes the capability of vitilig

259 We also show that the senescent phenotype is dynamic, changing at varying inte

260 s result from altered transcription, but the senescent phenotype is variable, and methods for clearly

261 nitiated after long-term FFD feeding reduces senescent phenotype markers in visceral adipose tissue w

262 e mechanisms by which Ras can promote such a senescent phenotype remain poorly defined.

263 ions are dependent on the development of the senescent phenotype, which involves an overproduction of

264 itor subpopulation characterised by an early senescent phenotype.

265 of proteasomes might be responsible for this senescent phenotype.

266 n normal proteasomal activity that mitigates senescent phenotypes induced by intensive cell replicati

267 us work indicating that redox state mediates senescent physiology in the hippocampus, the results ind

268 scribe fundamental metabolic requirements of senescent primary human CD8+ T cells and demonstrate tha

269 By using 9H4, we observed that senescent primary human fibroblasts express vimentin on

270 aling facilitates metastasis by generating a senescent, pro-inflammatory endothelium.

271 n A and directly inhibit adipogenesis in non-senescent progenitors.

272 d IL-4, and that these are also increased in senescent prostatic epithelial cells in vitro.

273 and counteracting aging through clearance of senescent proteins and mitochondria.

274 hepatocytes was investigated in juvenile and senescent rats deficient in dipeptidyl-peptidase IV.

275 ere significantly higher in juvenile than in senescent rats, suggesting that growth hormone might pro

276 rimary visual cortex (V1) of young adult and senescent rats.

277 ules in each red cell, and roughly 2 million senescent red cells are recycled each second.

278 ty with age (P = 0.029) that was specific to senescent skin cells.

279 other pro-senescence stimuli, as well as in senescent skin premalignant lesions.

280 Replicative senescent ST2 cells exhibited a strong association among

281 from the seedling to juvenile to mature and senescent stages.

282 henotype (SASP), which helps to maintain the senescent state and triggers bystander senescence in a p

283 Despite their apparent senescent state, we determined that these cells secreted

284 f the genome in defining and maintaining the senescent state.

285 Using this model, here we find that senescent stromal cells are sufficient to drive localize

286 To determine if senescent stromal cells influence tumorigenesis, we deve

287 k provides evidence that the accumulation of senescent stromal cells is sufficient to establish a tum

288 ases in immune cells that also localize near senescent stromal cells.

289 rning adaptive changes in senescing and post-senescent survivor yeast cells.

290 pus, which may represent the accumulation of senescent synapses with enhanced vulnerability to comple

291 rates the rate of accumulation of C1q-coated senescent synapses, enhancing synaptic vulnerability to

292 ts indicate that redox changes contribute to senescent synaptic function in vulnerable brain regions

293 inal increases in VZV-specific CD8(+)CD57(+) senescent T cells after vaccination, which were already

294 The proliferative defect of senescent T cells was reversed by blockade of AMPK-TAB1-

295 to accumulation of transitional B cells and senescent T cells, lymphadenopathy, and immune deficienc

296 hypothesized that an increased proportion of senescent, terminally differentiated CD8(+) T cells woul

297 males and females in driving these different senescent trends.

298 val than patients in which the proportion of senescent tumor cells did not change before and after tr

299 KA) with an MDM2 antagonist activates p53 in senescent tumors harboring wild-type 53.

300 l killer cells) associated with clearance of senescent tumors.