ライフサイエンスコーパス: senescent

1 can choose to remain proliferative or become senescent.

2 y exposed to chemotherapy but had never been senescent.

3 eded to determine if these cells are in fact senescent.

4 giocytes following pro-proliferative and pro-senescent (10-day lipopolysaccharide) stimulation.

5 cid fraction originates mainly in apoptotic, senescent and cancerous cells, this approach allows effi

6 tom bloom in the AASP and the sinking of the senescent and dead diatoms helps drive carbon sequestrat

7 and may contribute to a transition toward a senescent and fibroblastic NP cell with a limited capaci

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

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

10 can capture previously documented changes in senescent and progeria cells.

11 ing, we assessed changes in the methylome of senescent Arabidopsis (Arabidopsis thaliana) leaves indu

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

13 Senescent beta-catenin-depleted hepatocytes in aged mice

14 tantly, selective elimination of p16INK4a(+) senescent BM stromal cells in vivo improved the survival

15 te that ETS1 and p300 physically interact in senescent but not control NHCs.

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

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

18 Senescent cardiomyocytes exhibit a mismatch between ener

19 High levels of exhausted (PD-1+) and senescent (CD28null) CD4+ and CD8+ T cells were observed

20 sociated with an expansion of phenotypically senescent CD4+ and CD8+ T cells expressing CD57 and kill

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

22 Senescent CD8 + T cells, CD56 + T cells, CD56(dim) natur

23 ells decreased, naive B cells increased, and senescent CD8 T cells decreased (human cells); effects w

24 We also showed fewer anergic and senescent CD8(+) T cells in COVID-19 individuals, but no

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

26 arabiosis, pharmaceutical administration and senescent cell ablation.

27 Senescent cell accumulation in aging tissues is linked t

28 Indeed, senescent cell accumulation was presumably associated wi

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

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

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

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

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

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

35 Senescent cell extrinsic activities, broadly related to

36 the epigenetic state of enhancers determines senescent cell fate.

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

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

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

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

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

42 Senescent cell production occurs throughout life and pla

43 ndicating that persistent signaling supports senescent cell survival.

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

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

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

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

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

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

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

51 Senescent cells accumulate in human tissues during agein

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

53 Senescent cells affect many physiological and pathophysi

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

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

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 Senescent cells are characterized by an upregulation of

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

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

61 Senescent cells are thought to impair tissue function, a

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

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

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

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

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

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

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

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

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

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

72 Senescent cells contribute to both age-related degenerat

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

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

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

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

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

78 Accumulation of senescent cells during aging contributes to chronic infl

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

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

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

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

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

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

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

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

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

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

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

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

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

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

93 Senescent cells have undergone permanent growth arrest,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

112 Persistence of senescent cells is considered as a critical contributor

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

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

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

116 These senescent cells no longer divide but release multiple in

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

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

119 Senescent cells participate in a variety of physiologica

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

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

122 Senescent cells produce cytokines and chemokines, such a

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

124 Senescent cells release a melange of factors that drive

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

126 Senescent cells secrete a distinct set of factors, colle

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

128 Senescent cells secrete multiple inflammatory proteins k

129 Paradoxically, senescent cells secrete proinflammatory and growth-stimu

130 Senescent cells secrete several molecules, collectively

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

132 Senescent cells that accumulate in multiple tissues with

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

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

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

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

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

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

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

140 Senescent cells undergo a stable cell cycle arrest and p

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

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

143 Removal of senescent cells using senolytic drugs ameliorated cardia

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

160 In senescent cells, this selectively causes p53 nuclear exc

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

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

163 T cells to inhibit immune responses against senescent cells.

164 hich lead to the detrimental accumulation of senescent cells.

165 ither exclusively nor universally present in senescent cells.

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

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

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

169 selective markers to monitor the presence of senescent cells.

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

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

172 et engagement of senolytic agents that clear senescent cells.

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

174 that drives the transcriptional programme of senescent cells.

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

176 nished ATF6 nuclear localization in stressed senescent cells.

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

178 r results suggest that ETS1 and p300 promote senescent cholangiocyte resistance to apoptosis by modif

179 ic roles of these reactive proliferative and senescent cholangiocyte subpopulations in PSC.

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

181 ing BCL-xL-mediated, apoptosis resistance in senescent cholangiocytes and uncovered that ETS1 and the

182 Both ductular reactive cholangiocytes and senescent cholangiocytes can modify the periductal micro

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

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

185 for testing the induction and elimination of senescent chondrocytes, which will support investigation

186 cells were exposed to the SASP via in vitro senescent conditioned media (SCM) administration.

187 ining SWI/SNF complexes in proliferating and senescent conditions.

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

189 gbird with early life increases, followed by senescent declines, in survival and reproduction.

190 ed to die before reaching ages at which such senescent decreases could be observed.

191 Here we show that senescent dermal fibroblasts express the non-classical M

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

193 ether, the results suggest that clearance of senescent DRG neuronal cells following platinum-based ca

194 n, we found no evidence that nevus cells are senescent, either compared with other skin cells, or oth

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

196 show that microRNA-126 was downregulated in senescent endothelial cells and microvesicles.

197 We demonstrated that senescent endothelial cells experience impaired tube for

198 Senescent endothelial cells failed to express HIF-1alpha

199 The senescent endothelial cells resulted in pericyte loss an

200 re restored in HIF-1alpha stabilizer-treated senescent endothelial cells.

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

202 f the spleen mediate turnover of billions of senescent erythrocytes per day.

203 usion experiments, we further confirmed that senescent erythrocytes that are retained in the spleen a

204 ically activated on aged erythrocytes, cause senescent erythrocytes to interact with extracellular ma

205 Such adhesion molecule-driven retention of senescent erythrocytes under low shear conditions was fo

206 In contrast to intact senescent erythrocytes, the remnant erythrocyte ghost sh

207 ular mechanisms involved in sequestration of senescent erythrocytes, their recognition, and their sub

208 hemolysis as a key event in the turnover of senescent erythrocytes, which alters our current underst

209 GRSF1 expression was lower in senescent fibroblasts, and GRSF1 knockdown induced senes

210 a two-field composite consisting of a dermal senescent field driving the persistence of the overlying

211 However, senescent foliage falling from treated trees represents

212 In the SASP of cells that became senescent following several in vitro chemical and physic

213 c factors accompany the reprogramming of the senescent genome; however, the mechanism and extent of t

214 lpha-galactosylceramide increased removal of senescent hepatocytes by NKT cells.

215 Cxcr6(eGfp/eGfp) mice had significantly more senescent hepatocytes than livers of Nemo(LPC-KO) mice.

216 t NKT and CD4 T cells promote the removal of senescent hepatocytes to prevent hepatocarcinogenesis, a

217 diated NKT-cell and CD4(+) T-cell removal of senescent hepatocytes.

218 es in glucose uptake or lactate secretion in senescent HMECs.

219 olites into nucleotide synthesis pathways in senescent HMECs.

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

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

222 Depleting senescent HSCs by 'senolytic' treatment with dasatinib/q

223 found that COL3 was significantly reduced in senescent human mesenchymal stem cells and myofibroblast

224 ute two protein inhibitor, selectively kills senescent IVD cells through apoptosis.

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

226 nduce the reprogramming of non-proliferative senescent-like CD27(-)CD28(-)CD8(+) T cells to acquire a

227 KG2D and DAP12 and restored TCR signaling in senescent-like CD27(-)CD28(-)CD8(+) T cells.

228 The accumulation of senescent-like neuronal cells in DRG is associated with

229 Here, we show that cisplatin induces senescent-like neuronal cells in primary culture and in

230 To determine if depletion of senescent-like neuronal cells may effectively mitigate C

231 euronal cells reverses CIPN, suggesting that senescent-like neurons play a role in CIPN pathogenesis.

232 g, human and murine cardiomyocytes acquire a senescent-like phenotype characterised by persistent DNA

233 with bioenergetic changes and induction of a senescent-like phenotype.

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

235 essfully divide, the neuron instead enters a senescent-like state.

236 nd to be senescent, with increased levels of senescent markers and senescence-associated secretory ph

237 Additionally, senescent melanocyte SASP induces telomere dysfunction i

238 tudy provides proof-of-concept evidence that senescent melanocytes affect keratinocyte function and a

239 Finally, senescent melanocytes impair basal keratinocyte prolifer

240 Crucially, clearance of senescent melanocytes using the senolytic drug ABT737 or

241 D127(-)-resembling terminally differentiated senescent memory cells and CD127(+) CD57(-)-resembling p

242 Our findings reveal the importance of a senescent microenvironment for the pathophysiology of le

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

244 calcium leak and mitochondrial damage in the senescent myocardium.

245 by blocking pro-survival mechanisms, target senescent myofibroblast for apoptosis or promote the rep

246 ng evidence suggests that myofibroblasts and senescent myofibroblasts, rather than being resistant to

247 In line with senescent neural dedifferentiation more generally, our r

248 r results demonstrated that clearance of DRG senescent neuronal cells reverses CIPN, suggesting that

249 In senescent NHCs, TRAIL-mediated apoptosis was reduced ~70

250 Transcriptome analysis of OPCs revealed that senescent NPCs induced expression of epigenetic regulato

251 ent cells frequently engulf both neighboring senescent or nonsenescent tumor cells at a remarkable fr

252 Accumulation of senescent osteocytes contributes to deterioration of the

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

254 studies have examined the developmental and senescent phases together.

255 addition, we highlight the diversity of the senescent phenotype and its functional output beyond gro

256 gering DNA damage, growth suppression, and a senescent phenotype characterized by elevated production

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

258 Transient induction of a senescent phenotype has actually been suggested to promo

259 Transcriptomic analysis of the senescent phenotype identified a cell senescence signatu

260 Here, we report that AML blasts induce a senescent phenotype in the stromal cells within the BM m

261 Moreover, the senescent phenotype induced by DNA damage reagents, such

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

263 can ultimately lead to the acquisition of a senescent phenotype.

264 EGFR-1 expression and causing ECs to enter a senescent phenotype.

265 h drive fibroblasts toward a profibrotic and senescent phenotype.

266 that was found to be a primary driver of the senescent phenotype.

267 itor subpopulation characterised by an early senescent phenotype.

268 that the dermal field is characterized by a senescent phenotype.

269 + T cells toward a terminally differentiated/senescent phenotype.

270 They also exhibited senescent phenotypes and increased p53 expression.

271 roteins, including DGCR8, reversed premature senescent phenotypes in DR8(dex2) hMSCs.

272 Lange syndrome results in an inefficient and senescent placenta that impairs embryonic development.

273 ar senescence, and proliferation kinetics in senescent primary human fibroblasts.

274 we used LC-MS-based metabolomics to analyze senescent primary human mammary epithelial cells (HMECs)

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

276 thereby allowing condensin to contribute to senescent processes.

277 Significant reductions in proportions of senescent pulmonary CD28(-)CD57(+) CD8 T cells were obse

278 type in VICs that come into contact with the senescent RBCs of intraleaflet hematomas may play a crit

279 Senescent RBCs with reconstituted membranes were phagocy

280 ecognition marker, from the outer leaflet of senescent RBCs.

281 nstantly exposed to the blood flow, clearing senescent red blood cells (RBCs) and recycling iron from

282 Prior studies demonstrated that targeting senescent RGCs for removal (i.e., a senolytic approach)

283 racts with phosphatidylserine exposed on the senescent sickle red cell membrane.

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

285 nd accelerates the entry of SCs into a fully senescent state upon damage-induced stress.

286 expression in the quiescent, but not in the senescent, state.

287 Restoring extracellular matrix synthesis in senescent stem cells.

288 bubbles that carry signaling molecules, from senescent stromal cells can promote tumorigenesis and mu

289 The p16INK4a-expressing senescent stromal cells then feed back to promote AML bl

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

291 phenotypic and functional characteristics of senescent T cells and their role in human cancers.

292 was not significantly associated with these senescent T-cell phenotypes in this exploratory study of

293 with changes in these and other potentially senescent T-cell subsets.

294 tenance depends on continuous replacement of senescent taste cells with new ones generated by adult t

295 Placenta is a naturally senescent tissue; we demonstrate that persistent DNA dam

296 STP13 has a function in retrieving sugar in senescent tissues.

297 Cultured senescent tubular cells, kidneys of aged mice, and renal

298 nce-associated secretory phenotype (SASP) of senescent tumor cells through activation of matrix metal

299 Next, we find that the leukemia-driven senescent tumor microenvironment is caused by AML-induce

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

301 e resulting adipocytes were also found to be senescent, with increased levels of senescent markers an