ライフサイエンスコーパス: senescent cell

1 protein response (UPR) branches in stressed senescent cells.

2 cteristics of senescence can be found in non-senescent cells.

3 of newly synthesized H3.3 onto chromatin in senescent cells.

4 teins BCL-2 and BCL-xL and selectively kills senescent cells.

5 of the TGF-beta pathway that was impaired in senescent cells.

6 selective markers to monitor the presence of senescent cells.

7 e in fully quiescent differentiated cells or senescent cells.

8 emotherapy-treated cancer cells enriched for senescent cells.

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

10 idly identify drugs that specifically affect senescent cells.

11 a differentiation program characteristic of senescent cells.

12 rs in differentiating progenitors exposed to senescent cells.

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

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

15 dify the cellular markers characteristic for senescent cells.

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

17 et engagement of senolytic agents that clear senescent cells.

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

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

20 function, and suppress CCFs and the SASP in senescent cells.

21 that drives the transcriptional programme of senescent cells.

22 ation of the heat shock response in stressed senescent cells.

23 nished ATF6 nuclear localization in stressed senescent cells.

24 d bone loss that can be rescued by depleting senescent cells.

25 T cells to inhibit immune responses against senescent cells.

26 hich lead to the detrimental accumulation of senescent cells.

27 ither exclusively nor universally present in senescent cells.

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

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

30 s-systemic factors, metabolic manipulations, senescent cell ablation and cellular reprogramming-and d

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

32 arabiosis, pharmaceutical administration and senescent cell ablation.

33 Mounting evidence has established that senescent cells accumulate at sites of age-related patho

34 Senescent cells accumulate in aged tissue and are causal

35 Senescent cells accumulate in fat with aging.

36 Senescent cells accumulate in human tissues during agein

37 Senescent cells accumulate in human tissues, including t

38 Senescent cells accumulate in various tissues and organs

39 ee mitochondrial DNA (cf-mt-DNA) released by senescent cells accumulates with aging and augments immu

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

41 Senescent cell accumulation in aging tissues is linked t

42 Indeed, senescent cell accumulation was presumably associated wi

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

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

45 Senescent cells affect many physiological and pathophysi

46 or promotion, suggesting that elimination of senescent cells after chemotherapy may reduce occurrence

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

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

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

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

51 on type was also enriched in the treated pre-senescent cells, although to a lower extent.

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

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

54 t of old donor animals with senolytics clear senescent cells and diminish cf-mt-DNA release, thereby

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

56 x improvement correlated with a reduction in senescent cells and SASP, supporting a translational pot

57 racted investigative attention that revealed senescent cells and secreting proinflammatory and profib

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

59 Therefore, senescent cells and the SASP represent significant oppor

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

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

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

63 d and diabetic wounds had greater numbers of senescent cells, and diabetic macrophages maintained alt

64 nction was impaired following heat stress in senescent cells, and did not recover upon return to norm

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

66 protein exposing an epitope(s), probably the senescent cell antigen of band 3.

67 Senescent cells are characterized by an upregulation of

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

69 At present, senescent cells are identified by the combined presence

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

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

72 Based on the observation that senescent cells are large and exhibit many of the phenot

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

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

75 Senescent cells are thought to impair tissue function, a

76 Thus, we show for the first time that senescent cells are tumor promoters, not tumor initiator

77 rting a translational potential of targeting senescent cells as a therapeutic intervention.

78 hemotherapy-induced bone loss by identifying senescent cells as major drivers of bone loss and the p3

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

80 ons such as image-guided surgical removal of senescent cells, as well as the monitoring of drug-respo

81 yocytes and investigate whether clearance of senescent cells attenuates age-related cardiac dysfuncti

82 Identifying how senescent cells avoid apoptosis allows for the prospecti

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

84 mals, genetic and pharmacologic reduction of senescent cell burden results in the prevention, delay,

85 determine the effects of age and obesity on senescent cell burden; however, we were only able to ass

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

87 In senescent cells, but not proliferating cells, promoters

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

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

90 eoarthritis (OA) is to selectively eliminate senescent cells by initiating apoptosis.

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

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

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

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

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

96 c antigen receptor (CAR) T cells that target senescent cells can be effective senolytic agents.

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

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

99 The removal of senescent cells can improve lifespan and/or healthspan i

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

101 This adds another mechanism by which senescent cells can promote tumorigenesis and offers ano

102 cal process with progressive accumulation of senescent cells characterized by stable cell cycle arres

103 With increasing age, tissues accumulate senescent cells, characterized by an irreversible arrest

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

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

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

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

108 Senescent cells contribute to age-related tissue degener

109 Senescent cells contribute to both age-related degenerat

110 ly driver of OA, and the mechanisms by which senescent cells contribute to disease progression are no

111 umor suppression, whereas the persistence of senescent cells contributes to aspects of aging.

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

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

114 ically, thymic atrophy is thought to reflect senescent cell death, while regeneration requires prolif

115 hese results indicate that BCL-xL provides a senescent cell death-inducing or senolytic target that m

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

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

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

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

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

121 st cancer and limits fibrosis, but lingering senescent cells drive age-related disorders.

122 by suggesting a new strategy for eliminating senescent cells during ageing.

123 Accumulation of senescent cells during aging contributes to chronic infl

124 populations including airway stem cells and senescent cells emerging during pulmonary fibrosis.

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

126 Thus, the accurate detection of senescent cells, especially in vivo, is essential.

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

128 ellular metabolite pool sizes indicated that senescent cells exhibit depletion of metabolites from nu

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

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

131 permit ganciclovir (GCV) to selectively kill senescent cells expressing herpes simplex virus 1 thymid

132 ies have shown that depletion of chronically senescent cells extends healthy lifespan and delays age-

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

134 Senescent cell extrinsic activities, broadly related to

135 the epigenetic state of enhancers determines senescent cell fate.

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

137 tions to prevent senescence and to eliminate senescent cells for prevention of vascular pathologies a

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

139 mors, we show here that chemotherapy-induced senescent cells frequently engulf both neighboring senes

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

141 Accordingly, eliminating senescent cells from damaged tissues in mice ameliorates

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

143 tic treatment of AD mice selectively removed senescent cells from the plaque environment, reduced neu

144 feasibility and safety to selectively ablate senescent cells from tissues, a therapeutic modality tha

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

146 Pathologically, the aberrant accumulation of senescent cells generates an inflammatory milieu that le

147 In senescent cells, H4K20me3 is especially enriched at DNA

148 ere treated with conditioned media (CM) from senescent cells had increased MerTK cleavage, impaired e

149 Ablation of senescent cells has been postulated as a promising thera

150 Senescent cells have a distinct gene expression profile,

151 Recently, senescent cells have been observed in glaucomatous eyes,

152 Senescent cells have undergone permanent growth arrest,

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

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

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

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

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

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

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

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

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

162 However, the dynamic interplay of senescent cells in diabetic wounds is not well understoo

163 the present study, we attempted to identify senescent cells in frozen human skeletal muscle biopsies

164 utic avenues that may be exploited to target senescent cells in future geriatric medicine.

165 nsistently, HLA-E expression is increased on senescent cells in human skin sections from old individu

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

167 (OA) correlates with a rise in the number of senescent cells in joint tissues, and the senescence-ass

168 Frequencies of senescent cells in liver and intestinal crypts quantitat

169 Pharmacological or genetic clearance of senescent cells in mice alleviates detrimental features

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

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

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

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

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

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

176 We found a significant increase of senescent cells in the lungs, heart, and kidneys of mice

177 chanisms contributing to the accumulation of senescent cells in the skin and how the persistence of c

178 functions require the transient presence of senescent cells in the tissue microenvironment.

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

180 A-E expression contributes to persistence of senescent cells in tissues, thereby suggesting a new str

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

182 uPAR-specific CAR T cells efficiently ablate senescent cells in vitro and in vivo.

183 -E and NKG2A boosts immune responses against senescent cells in vitro.

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

185 e profiles will enable the identification of senescent cells in vivo, the investigation of their role

186 identification and selective elimination of senescent cells in vivo, to the well-established two-ste

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

188 riginating stimulus, and tissue of origin of senescent cells in vivo.

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

190 profiling of IL-1 receptor (IL-1R)-depleted senescent cells indicates that IL-1 controls the late ar

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

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

193 In preclinical aging models, accumulation of senescent cells is associated with multiple chronic dise

194 Persistence of senescent cells is considered as a critical contributor

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

196 Cell cycle arrest in SETD1A knockdown senescent cells is independent of mutations in p53, RB a

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

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

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

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

201 rogram of engulfment in chemotherapy-induced senescent cell lines and tumors.

202 of splicing factor expression, reduction in senescent cell load, and partial reversal of multiple ce

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

204 Recent studies using senescent cell manipulation and depletion as novel thera

205 ceptor (CAR)-T cells targeting uPAR, a novel senescent-cell marker, to treat liver adenocarcinoma and

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

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

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

209 Senescent cells may promote tumour progression through t

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

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

212 These senescent cells no longer divide but release multiple in

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

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

215 peutically using 'senolytic' drugs that kill senescent cells or inhibitors of the senescence-associat

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

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

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

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

220 Given the heterogeneity of senescent cells, our knowledge of both the drivers and c

221 Senescent cells participate in a variety of physiologica

222 data suggest compelling explanations for how senescent cells persist in dormancy, how they manage the

223 As senescent cells persist in tissues, they cause local inf

224 CD8+ and CD4+ T-cells expressing CD28-CD57+ (senescent cell phenotype).

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

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

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

228 Senescent cells produce cytokines and chemokines, such a

229 Senescent cell production occurs throughout life and pla

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

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

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

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

234 Ablation of senescent cells reduced p38MAPK and MAPK/ERK signaling,

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

236 Senescent cells release a melange of factors that drive

237 ch constitute a large portion of accumulated senescent cells, release a senescence-associated secreto

238 diseases, yet senolytic therapies targeting senescent cells remain hindered by lack of specificity.

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

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

241 Small molecules that selectively kill senescent cells (SCs), termed senolytics, have the poten

242 ion and the accumulation of pro-inflammatory senescent cells (SCs).

243 Senescent cells secrete a distinct set of factors, colle

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

245 Senescent cells secrete cytokines and other factors of t

246 Senescent cells secrete multiple inflammatory proteins k

247 Paradoxically, senescent cells secrete proinflammatory and growth-stimu

248 Senescent cells secrete several molecules, collectively

249 Senescent cells secrete various growth factors and cytok

250 Senescent cells secrete various growth factors, cytokine

251 nt in LGs after the selective elimination of senescent cells (senolysis) with ABT-263.

252 1, elevated in dividing cells and reduced in senescent cells, sequesters let-7 to enable a proliferat

253 al and transcriptional regulatory responses, senescent cells showed enhanced translational regulation

254 Senescent cells (SnCs) accumulate in many vertebrate tis

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

256 ndicating that persistent signaling supports senescent cell survival.

257 identifying compounds that selectively kill senescent cells (termed senolytics).

258 While drugs that selectively kill senescent cells, termed "senolytics" are a major focus,

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

260 Senescent cells that accumulate in multiple tissues with

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

262 tumorigenesis and offers another activity of senescent cells that might be targeted to limit the spre

263 drugs that specifically target the "benign" senescent cells that surround and support AML.

264 and the development of strategies to target senescent cells therapeutically.

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 Thus, targeting senescent cells to delay aging and limit dysfunction, kn

269 pically transplanted ex vivo therapy-induced senescent cells to immune checkpoint blockade in vivo.

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

271 cs and senomorphics) that eliminate or alter senescent cells to stop disease progression and pathogen

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

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

274 agments (CCFs), extruded from the nucleus of senescent cells, trigger the SASP through activation of

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

276 Senescent cells undergo a stable cell cycle arrest and p

277 Senescent cells undergo dramatic alterations to their ch

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

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

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

281 Removal of senescent cells using senolytic drugs ameliorated cardia

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

283 predominant mutation type in the treated pre-senescent cells was G:C->T:A transversion, whose frequen

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

285 Senescent cells were positive for platelet-derived growt

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

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

288 However, in senescent cells where PANDA sequesters transcription fac

289 tive cII mutant frequency in the treated pre-senescent cells which was augmented in their immortalize

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

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

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

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

294 Recent evidence demonstrates that senescent cells, while initially restricting tumorigenes

295 ce to promote metastasis, and elimination of senescent cells with a senolytic BCL-2 inhibitor impairs

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

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

298 nhibiting specific miRNAs, or by deletion of senescent cells with senolytic therapies, already shown

299 inability to identify and isolate individual senescent cells within an intact organism.

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