ライフサイエンスコーパス: senescent cell

1 rs in differentiating progenitors exposed to senescent cells.

2 selective markers to monitor the presence of senescent cells.

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

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

5 dify the cellular markers characteristic for senescent cells.

6 r ADAM17 in shaping the secretory profile of senescent cells.

7 ic stem cells as a source of replacement for senescent cells.

8 -associated CD8+ T lymphocytes also harbored senescent cells.

9 uired for the induction of p21 expression in senescent cells.

10 reased level of chromatin-associated BRG1 in senescent cells.

11 agy/lysosomal pathway processes chromatin in senescent cells.

12 xpression, we examined the nuclear lamina of senescent cells.

13 ession was validated in proliferative versus senescent cells.

14 tes of tubular cells and significantly fewer senescent cells.

15 2A.X, and consequently a decreased number of senescent cells.

16 tion factor that accumulates on chromatin of senescent cells.

17 o cancer and it is linked to the presence of senescent cells.

18 ment, and trigger immune surveillance of the senescent cells.

19 on cell proliferation and iROS production in senescent cells.

20 about how CDK5 is activated in non-neuronal senescent cells.

21 s properly functioning tissue is replaced by senescent cells.

22 methylation, and by an increased fraction of senescent cells.

23 and include particles such as pathogens and senescent cells.

24 levels, and hypoxia further induced VEGF in senescent cells.

25 lelic variation and ultra-short telomeres in senescent cells.

26 and more resistance to oxidative damage than senescent cells.

27 this switch to biallelic IGF2 expression in senescent cells.

28 s associated with reduced CTCF expression in senescent cells.

29 -ras-induced senescent cells and replicative senescent cells.

30 e with gammaH2AX-positive DNA damage foci in senescent cells.

31 s is a process that produces timely death in senescent cells.

32 g pRb activity to cytoskeletal regulation in senescent cells.

33 e in fully quiescent differentiated cells or senescent cells.

34 emotherapy-treated cancer cells enriched for senescent cells.

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

36 idly identify drugs that specifically affect senescent cells.

37 a differentiation program characteristic of senescent cells.

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

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

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

41 Senescent cells accumulate in aged tissue and are causal

42 Although senescent cells accumulate in elderly individuals, most

43 Senescent cells accumulate in fat with aging.

44 Senescent cells accumulate in human tissues, including t

45 Here we show that senescent cells accumulate in murine livers treated to p

46 Senescent cells accumulate in various tissues and organs

47 Senescent cells accumulate in various tissues and organs

48 In particular, many senescent cells accumulate specialized domains of facult

49 Because senescent cells accumulate with age, their presence is h

50 entually limiting longevity as dysfunctional senescent cells accumulate.

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

52 Senescent cell accumulation in aging tissues is linked t

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

54 Nonetheless, senescent cells acquire phenotypic changes that may cont

55 Senescent cells acquire the 'senescence-associated secre

56 These results suggest that senescent cells activate a self-amplifying secretory net

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

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

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

60 Senescent cells also acquire a complex phenotype that in

61 Senescent cells also secrete growth factors, proteases,

62 Senescent cells also secrete inflammatory cytokines such

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

64 in control of chromatin in nonproliferating senescent cells, although its role is poorly defined.

65 ble phagocytic "eat me signal" to facilitate senescent cell and oxidized lipoprotein recognition by t

66 in fragments are released from the nuclei of senescent cells and are subsequently targeted for proces

67 expression induced a significant increase in senescent cells and decrease in apoptotic cells.

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

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

70 st recorded allelic distribution (300 bp) in senescent cells and displayed a general, but not absolut

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

72 Nf1+/- MSPC also have fewer senescent cells and have a significantly higher telomera

73 as identified initially as a gene induced in senescent cells and itself has been shown to cause perma

74 sive production of inflammatory mediators in senescent cells and limit their deleterious effects on t

75 e regulators in both oncogenic H-ras-induced senescent cells and replicative senescent cells.

76 sponse factors were assembled in a subset of senescent cells and signaled through ATM to p53, upregul

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

78 he phosphorylation of the ATR target CHK1 in senescent cells and the response of ATM-deficient cells

79 Therefore, senescent cells and the SASP represent significant oppor

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

81 therapeutic opportunities based on targeting senescent cells and the SASP, and potential paths to dev

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

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

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

85 r cellular digestion of microbial pathogens, senescent cells, apoptotic bodies, and retinal outer seg

86 However, whether senescent cells are causally implicated in age-related d

87 The senescent cells are derived primarily from activated hep

88 tumor suppression, yet the dynamics by which senescent cells are formed, their effects on tissue func

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

90 Senescent cells are irreversibly growth-arrested and sho

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

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

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

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

95 Senescent cells are thought to impair tissue function, a

96 any of them bypass mitosis and become single senescent cells as evidenced by the expression of senesc

97 15-LOX2 mice) showed a dramatic increase in senescent cells as revealed by increased SA-betagal, p27

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

99 Identifying how senescent cells avoid apoptosis allows for the prospecti

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

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

102 In senescent cells, but not proliferating cells, promoters

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

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

105 adhesion molecule 1 (ICAM1) is released from senescent cells by microvesicles independently of ADAM17

106 to the irreversible cell cycle exit in many senescent cells by repressing the expression of prolifer

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

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

109 Senescent cells can accumulate senescence-associated het

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

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

112 enotype, we generated a mouse model in which senescent cells can be visualized and eliminated in livi

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

114 Senescent cells can give rise to survivors that maintain

115 However, accumulating evidence shows that senescent cells can have deleterious effects on the tiss

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

117 s are by definition eliminated from tissues, senescent cells can persist, acquire altered functions,

118 g age-related phenotypes and that removal of senescent cells can prevent or delay tissue dysfunction

119 tivation of DNA damage checkpoint kinases in senescent cells can restore cell-cycle progression into

120 introduction of wild-type p16(INK4A) in post-senescent cells caused growth arrest.

121 HOTAIR levels are highly upregulated in senescent cells, causing rapid decay of targets Ataxin-1

122 s displayed an age-dependent accumulation of senescent cells (CD28-CD57+) with decreased Delta133p53

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

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

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

126 Active Ras was reduced in Sirtinol-treated senescent cells compared with untreated cells.

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

128 We also show that senescent cells contain activated forms of the DNA damag

129 Senescent cells contribute to age-related tissue degener

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

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

132 through p53, up-regulating p21, and causing senescent cell-cycle arrest.

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

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

135 sized histones H3.3 and H4 into chromatin of senescent cells depends on HIRA.

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

137 Senescent cells develop characteristic morphological cha

138 roaches, we show that the chromosome ends of senescent cells directly contribute to the DNA damage re

139 Senescent cells display gene expression patterns that re

140 Although senescent cells do not proliferate, they remain metaboli

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

142 ng yeast Saccharomyces cerevisiae (young and senescent cells), Drosophila (embryonic cycles 10 and 14

143 sequences on the generation of replicatively senescent cells during organismal aging.

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

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

146 Senescent cells exhibited markers of lysosomal-mediated

147 o replicative senescent cells, H-ras-induced senescent cells exhibited specific downregulation of gen

148 ADPH oxidase 1 enzyme complex, whereupon the senescent cells express an antifibrosis genetic program.

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

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

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

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

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

154 ation growth rate, and higher percentages of senescent cells from passage 5 (P5) to P7 than their wil

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

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

157 understanding of the mechanisms that control senescent-cell gene expression programs has also recentl

158 Similar to replicative senescent cells, H-ras-induced senescent cells exhibited

159 In senescent cells, H4K20me3 is especially enriched at DNA

160 Senescent cells have a distinct gene expression profile,

161 elieved to have a tumor suppressor function, senescent cells have been shown to increase the potentia

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

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

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

165 an nevi are a paradigm for tumor-suppressive senescent cells in a premalignant neoplasm.

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

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

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

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

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

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

172 mor-inhibiting M1-state capable of attacking senescent cells in culture, whereas proliferating p53-de

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

174 Frequencies of senescent cells in liver and intestinal crypts quantitat

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

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

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

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

179 development of fibrosis and accumulation of senescent cells in the lung via a mechanism dependent up

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

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

182 g-induced conversion of T cells and DCs into senescent cells in vitro and in vivo.

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

184 telomere shortening and further increase in senescent cells in vivo, providing a mechanism for the v

185 revealed various layers of functionality of senescent cells in vivo.

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

187 Instead, p38 MAPK blockade in these senescent cells induced an increase in autophagy through

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

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

190 The cancer-promoting activity of senescent cells is likely due to secreted molecules, the

191 Expression of tumor-promoting factors by senescent cells is mediated, at least in part, by senesc

192 lopment, suggesting that the accumulation of senescent cells is not a principal determinant of cancer

193 ow the SAHF assembly pathway is activated in senescent cells is not known.

194 A characteristic of senescent cells is the heterochromatinization of loci en

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

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

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

198 In senescent cells, lamin A/C-negative, but strongly gamma-

199 rance of the G-rich 3' telomeric overhang in senescent cells led to the hypothesis that loss of the 3

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

201 , conditioned medium from IL-1alpha-depleted senescent cells markedly reduced the IL-6/IL-8-dependent

202 talloproteinase (MMP)-1, an inflammation and senescent cell marker, at the mRNA and protein levels, w

203 n levels, whereas the induction of two other senescent cell markers is either weak (interleukin-8) or

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

205 the mechanisms that control the viability of senescent cells may be helpful in eliminating these cell

206 origenesis in vivo and support the idea that senescent cells may facilitate age-associated cancer dev

207 ings show that, under certain circumstances, senescent cells may favor tumor progression because of t

208 determine the pattern of gene expression in senescent cells may lead to more effective treatments fo

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

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

211 ased on the present results, we propose that senescent cells may promote cancer growth both by a dire

212 Senescent cells may promote tumour progression through t

213 n senescent cells, suggesting that young and senescent cells may use different end joining pathways.

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

215 Enriched within atherosclerotic plaque and senescent cell membranes, oxPC(CD36) promote the uptake

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

217 ompanied by the appearance of characteristic senescent cell morphology and senescence-associated acid

218 homeostatic levels, an equivalent number of senescent cells must be cleared from circulation.

219 ted recruitment of HP1gamma occurred in only senescent cells, not in quiescent cells; thus, there is

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

221 Senescent cells often express p16(INK4a), a cyclin-depen

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

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

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

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

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

227 In senescent cells, p95HER2 elicits a secretome enriched in

228 Senescent cells participate in a variety of physiologica

229 pamycin inhibitor, rapamycin, suppresses the senescent cell phenotype and extends life span in divers

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

231 une exhaustion phenotype rather than PD-1 or senescent cells plays an important role in age-related T

232 h a bias towards either the proliferating or senescent cell populations depending on the cell line.

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

234 We conclude that senescent cells process their chromatin via an autophagy

235 Senescent cell production occurs throughout life and pla

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

237 ence secretome, we show that p95HER2-induced senescent cells promote metastasis in vivo in a non-cell

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

239 In this paracrine fashion, senescent cells promoted invasion by inducing an epithel

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

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

242 s reduced up to 4.5 fold in presenescent and senescent cells, relative to young cells.

243 nisms underlying caveolin-1 up-regulation in senescent cells remain unknown.

244 letion-mediated interactions contributing to senescent cell removal from the circulation.

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

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

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

248 Senescent cells secrete altered levels of growth factors

249 Senescent cells secrete cytokines and other factors of t

250 ion of potentially oncogenic cells, and most senescent cells secrete high levels of proinflammatory c

251 Senescent cells secrete multiple growth-regulatory prote

252 Senescent cells secrete various growth factors and cytok

253 Senescent cells secrete various growth factors, cytokine

254 1, elevated in dividing cells and reduced in senescent cells, sequesters let-7 to enable a proliferat

255 Senescent cells (SnCs) accumulate in many vertebrate tis

256 In senescent cells, specialized domains of transcriptionall

257 Our findings may in part explain why senescent cells stimulate tumorigenesis in vivo and supp

258 silencing of retinoblastoma target genes in senescent cells, suggesting a mechanism by which retinob

259 elevated DNA damage response or evidence of senescent cells, suggesting an altered balance between g

260 omologies for end joining was compromised in senescent cells, suggesting that young and senescent cel

261 ndicating that persistent signaling supports senescent cell survival.

262 Gene expression patterns in the senescent cell suspension cultures are more similar to t

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

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

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

266 In senescent cells, this selectively causes p53 nuclear exc

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

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

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

270 Conditioned medium from senescent cells treated with antioxidants or Ca(2+) chel

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

272 Senescent cells undergo a stable cell cycle arrest contr

273 Senescent cells undergo dramatic alterations to their ch

274 inducible elimination of p16(Ink4a)-positive senescent cells upon administration of a drug.

275 round, INK-ATTAC removes p16(Ink4a)-positive senescent cells upon drug treatment.

276 rmal hyperplasia prevented the appearance of senescent cells upon p14(ARF) induction.

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

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

279 on of selected proteins and fragments in the senescent cells versus control ARPE-19 cells was achieve

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

281 proliferation index as well as apoptotic and senescent cells were detected in the lesions of mice wit

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

283 Senescent cells were identified by the expression of the

284 In addition, a substantial number of senescent cells were observed among both thymocytes and

285 her proliferation rate and reduced number of senescent cells were observed in MSCs lacking p85alpha c

286 Senescent cells were positive for platelet-derived growt

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

288 However, once formed, senescent cells were retained in the epidermis, often fo

289 Whole senescent cells were then treated with deuterated D(3)-a

290 However, in senescent cells where PANDA sequesters transcription fac

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

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

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

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

295 One proposed factor is the presence of senescent cells, which increase with age.

296 Senescent cells, while not dividing, remain metabolicall

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

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

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

300 eal the potential for prolonged retention of senescent cells within tissues.