ライフサイエンスコーパス: cell senescence

1 ion and eventually signal cell cycle arrest (cell senescence).

2 by continuous passaging induced replicative cell senescence.

3 ident self-renewing cells by preventing stem cell senescence.

4 , is associated with vascular DNA damage and cell senescence.

5 a critical length is achieved, precipitating cell senescence.

6 xpression of cell cycle inhibitors and tumor cell senescence.

7 beta-galactosidase staining, an indicator of cell senescence.

8 vin, which resulted in growth inhibition and cell senescence.

9 e-stabilizing agent that induces accelerated cell senescence.

10 ved GFR, decreased sclerosis, and alleviated cell senescence.

11 MP-1 up-regulation with the establishment of cell senescence.

12 e activation of endogenous wild-type p53 and cell senescence.

13 telomeric circles, telomere shortening, and cell senescence.

14 em cell number and an increase in progenitor cell senescence.

15 asis decay as a key contributing effector of cell senescence.

16 imulate p53 acetylation and the induction of cell senescence.

17 functionally dependent on p53 in regulating cell senescence.

18 of Rac1 in regulating genomic stability and cell senescence.

19 ght be associated with its ability to induce cell senescence.

20 ersible growth arrest in the early stages of cell senescence.

21 re resistant to apoptosis, growth arrest and cell senescence.

22 n of flat cells, growth arrest, and finally, cell senescence.

23 ty genes for this disease, confer risk for T cell senescence.

24 sions in culture, a state termed replicative cell senescence.

25 ase in normal fibroblasts appears to prevent cell senescence.

26 at the ends of chromosomes, plays a role in cell senescence.

27 nt role for p27(Kip1) in promoting satellite cell senescence.

28 chanism without the complementary process of cell senescence.

29 ues, and this process has been implicated in cell senescence.

30 cultured OPCs to aggregating Abeta triggered cell senescence.

31 ed to the telomere hypothesis of replicative cell senescence.

32 sponses as cell cycle arrest, apoptosis, and cell senescence.

33 rved between the average telomere length and cell senescence.

34 be a cause rather than just a consequence of cell senescence.

35 opic GATA4 expression results in lung cancer cell senescence.

36 on of diminished therapeutic efficacy due to cell senescence.

37 -cell modulation in vivo, with evidence of T-cell senescence.

38 e mice with insights into pulmonary vascular cell senescence.

39 ific organ injury and immunosuppression on T-cell senescence.

40 gate graft-versus-host disease by inducing T-cell senescence.

41 cognitive function, in addition to reducing cell senescence.

42 molecular mechanisms that induce endothelial cell senescence.

43 a role in counteracting telomere erosion or cell senescence.

44 9), and IL-9 blockade prevented ILC-driven T-cell senescence.

45 A(2) activity in responder T cells during T cell senescence.

46 e age-related pathologies by preventing stem cell senescence.

47 yofibroblasts and epithelial stem/progenitor cell senescence.

48 ied by double-strand breaks, DNA damage, and cell senescence.

49 ung capillary rarefaction due to endothelial cell senescence.

50 or LBP and other painful disorders linked to cell senescence.

51 WNT7B downregulation and eventually triggers cell senescence.

52 They then explore telomere biology and cell senescence.

53 s was associated with increased osteoblastic cell senescence.

54 elomere attrition, altered proteostasis, and cell senescence.

55 ance circumvents destructive, stress-induced cell senescence.

56 ation and colony formation but induced tumor cell senescence.

57 ion induces p16(INK4A) and p14(ARF)-mediated cell senescence.

58 growth of MSCs, which developed features of cell senescence.

59 and DNA repair, or can trigger apoptosis or cell senescence.

60 premature chromatin changes and accelerated cell senescence.

61 ltered cell metabolism is also a hallmark of cell senescence, a condition characterized by loss of pr

62 Cell senescence, a putative tumor-suppression mechanism,

63 Ercc1(d/-) mice showed increased vascular cell senescence, accelerated development of vasodilator

64 t evidence on molecular characteristics of T-cell senescence affecting alloimmunity and organ quality

65 There were no changes in markers of CD8(+) T-cell senescence after ART and no differential changes in

66 transcriptionally upregulated in models of B-cell senescence, aging, insulin resistance, and T2D.

67 T cell senescence alters the homeostasis of distinct T cel

68 n of mitochondrial homeostasis could lead to cell senescence, although the underlying mechanism remai

69 link between these responses in endothelial cell senescence and a potential contribution to microvas

70 data strengthen the potential link between T-cell senescence and age-related neurodegenerative diseas

71 omere protection occurs during physiological cell senescence and ageing, due to attrition of telomeri

72 t that cAMP-elevating agents prevent cumulus cell senescence and allow them to continue to exert bene

73 adiation, even at low dose-rates, can induce cell senescence and alter gene expression via a hitherto

74 Telomere attrition induces cell senescence and apoptosis.

75 ession is accompanied by the upregulation of cell senescence and apoptotic markers.

76 ACTH expression, induces corticotroph tumor cell senescence and cell cycle exit by up-regulating p27

77 re, we have demonstrated that P2Y14 modifies cell senescence and cell death in response to tissue str

78 interpretation of vicarious relation between cell senescence and CKD may expand the arsenal of pharma

79 that by targeting NOX2 we reduced BM stromal cell senescence and consequently reduced AML proliferati

80 lated to neurogenesis, telomere maintenance, cell senescence and cytokine production.

81 fied several significant genes involved in T-cell senescence and cytotoxicity, consistent with T-cell

82 ential feature of cancer is dysregulation of cell senescence and death.

83 , including stress resistance, adipogenesis, cell senescence and energy production.

84 Despite T cell senescence and enhanced T cell activation, T cell A

85 tauopathy, which may arise from endothelial cell senescence and eNOS dysfunction triggered by intern

86 al hip BMD loss, whereas markers of CD4(+) T-cell senescence and exhaustion (CD4(+)CD28(-)CD57(+)PD1(

87 T cell senescence and exhaustion are major barriers to suc

88 hronic infection and found evidence of CD4 T cell senescence and exhaustion.

89 se by inducing ssDNA formation, driving host cell senescence and facilitating infection.

90 rested cells displayed phenotypic markers of cell senescence and failed to form colonies.

91 process that is essential for normal papilla cell senescence and flower receptivity.

92 ) T cell antitumor function by restraining T cell senescence and functional exhaustion through epigen

93 ivity mimicking levels in PDAC led to acinar cell senescence and generated inflammation and fibrosis

94 JNK2 prevents Ras-induced cell senescence and growth arrest by reducing the expres

95 ntigen receptor group (DARC), inducing tumor cell senescence and interrupting IL-8-mediated vascular

96 specific inhibitor 3-DZNeP promotes tubular cell senescence and kidney aging characterized by an inc

97 Renal epithelial cell senescence and kidney aging have become the focus o

98 es (T2D), increasing the probability of beta cell senescence and leading to reduced cell mass and dec

99 ng G1 phase cell-cycle arrest accompanied by cell senescence and let-7 inducing G2-M phase cell-cycle

100 mere length, which are known determinants of cell senescence and longevity, in peripheral blood monon

101 the pathogenesis of AGA both in relation to cell senescence and migration but also secretion of know

102 of genes associated with various aspects of cell senescence and organism aging.

103 nding renal aging, focusing on mechanisms of cell senescence and possible interventions to modulate a

104 red muscle growth, associated with satellite cell senescence and premature sarcopenia.

105 sults establish EGR1 as a major regulator of cell senescence and previously undescribed upstream "gat

106 TERT protein expression, and induced cancer-cell senescence and proliferative arrest.

107 s responsible for ionizing radiation-induced cell senescence and protection against oncogene-induced

108 uppression that induces targeted responder T-cell senescence and provide new insights relevant for th

109 indings identify mechanistic links between T cell senescence and regulation of lipid metabolism in th

110 Importantly, silencing CircPVT1 promoted cell senescence and reversed the proliferative phenotype

111 t the cellular level, JunB induced epidermal cell senescence and slowed cell growth in a cell-autonom

112 Oxidative stress can promote cell senescence and studies have shown a role for oxidat

113 xtensively shared with miR-155 to restrain T cell senescence and sustain CD8(+) T cell antitumor resp

114 tic activity of telomerase, causing the same cell senescence and telomere shortening phenotypes as a

115 d that BAP1 interaction with ASXL2 regulates cell senescence and that ASXL2 cancer-associated mutatio

116 teract to promote retinal pigment epithelial cell senescence and that bone morphogenetic protein-4 ma

117 We propose that cell senescence and the associated secretory phenotype c

118 family) and p53 regulate cell proliferation, cell senescence, and apoptosis in many cell types.

119 hondrial DNA damage, including inflammation, cell senescence, and apoptosis, are present in vascular

120 ssor responses such as cell differentiation, cell senescence, and apoptosis.

121 ritically short telomeres produce apoptosis, cell senescence, and chromosomal instability in tissue c

122 of p53 in DNA damage-induced growth arrest, cell senescence, and direct CDK regulation.

123 up-regulation, pattern recognition receptor, cell senescence, and immune response pathway activation

124 ster oxidative stress, platelet aggregation, cell senescence, and inflammatory responses in endotheli

125 ow release and progression to normal myeloid cell senescence, and not a direct effect of activation o

126 part, is a result of increased osteoblastic cell senescence, and that ST-SPI diet early in life has

127 part, is a result of increased osteoblastic cell senescence, and that ST-SPI diet early in life has

128 age, the functional consequences of vascular cell senescence, and the possibility that preventing acc

129 in advanced lesions, whereas VSMC apoptosis, cell senescence, and VSMC-derived macrophage-like cells

130 ssion and instability, in part, by promoting cell senescence, apoptosis, and inflammation, the direct

131 es by nutrient starvation without activating cell senescence, apoptosis, or a death-related p53 canon

132 erentiation of the cell to a specific immune cell, senescence, apoptosis, and many more.

133 Mitochondrial dysfunction and cell senescence are hallmarks of aging and are closely i

134 n target of rapamycin complex 1 (mTORC1) and cell senescence are intimately linked to each other and

135 been proposed that the genes responsible for cell senescence are located near the telomere and are ac

136 al. employed bioinformatics to characterize cell senescence as a primary factor in the common pathog

137 microbial pathophysiology and mechanisms of cell senescence as important mechanistic links to cancer

138 nse to stress, viral defense, apoptosis, and cell senescence as well as protein sequestration, modifi

139 Finally, cell senescence, as assessed by senescence-associated be

140 These data provide the first evidence of cell senescence, as represented by CD31+CD28(null) CD8+

141 monary arterial remodeling through increased cell senescence, as well as vascular tone alterations be

142 n of Hsp72 in certain cancer lines triggered cell senescence associated with activation and stabiliza

143 anced cytokine production, and upregulated T-cell senescence-associated surface receptors (CD57, KLRG

144 e present a consensus from the International Cell Senescence Association (ICSA), defining and discuss

145 ocesses, such as apoptosis, redox responses, cell senescence, autophagy, and iron homeostasis.

146 nfkb1(-/-) fibroblasts exhibit aggravated cell senescence because of an enhanced autocrine and par

147 s were normal up to 30 PDs, with significant cell senescence beginning following 35 PDs.

148 IRIF persistence and increased breast cancer cell senescence both in vitro and in vivo, arguing for t

149 teractive association of kidney diseases and cell senescence, both culminating in progressive deterio

150 ncroachment of underlying kidney disease and cell senescence bring about the conclusion that both ent

151 erase enables stem and cancer cells to evade cell senescence by adding telomeric sequences to the end

152 nterestingly, the induction of hematopoietic cell senescence by IR, but not by BU, was associated wit

153 ling pathways responsible for induction of T cell senescence by malignant tumors, and then discuss po

154 r cells of the hematopoietic system inhibits cell senescence by monitoring and responding to the extr

155 tissues, rapamycin prevents epithelial stem cell senescence by reducing oxidative stress through inc

156 Increased frequency of donor-specific T cell senescence, C4d deposition, and higher density of i

157 Importantly, cell senescence can also change or hamper response to di

158 Therapeutics that induce cancer cell senescence can block cell proliferation and promote

159 We also discuss how endothelial cell senescence causes arterial dysfunction and contribu

160 According to the telomere hypothesis of cell senescence, cells eventually reach a critically sho

161 T-cell senescence, characterized by expansion of cells lac

162 at cellular processes such as damage-induced cell senescence contribute to osteoarthritis and a growi

163 Therefore, prevention of beta cell senescence could reduce the risk of diabetes.

164 Cell senescence (CS) is at the nexus between aging and a

165 in hepatocytes induces massive p53-dependent cell senescence/death.

166 ery of PML bodies and revealed their role in cell senescence, disease pathogenesis, and responsivenes

167 Hallmarks of ageing include evidence of cell senescence, DNA damage (including telomere attritio

168 -mediated induction of cell cycle arrest and cell senescence) does not recapitulate the tumor suscept

169 Here, we report that development of T cell senescence driven by both malignant tumor cells and

170 e T cell-mediated autoimmune process in beta-cell senescence during T1D.

171 verse and highly complex role of cell death, cell senescence, endoplasmic reticulum stress, autophagy

172 high module scores for pathways involved in cell senescence, epithelial-mesenchymal transition, and

173 differential roles of CD4(+) versus CD8(+) T-cell senescence/exhaustion and effects of antiretroviral

174 markers on CD8 + T cells, an indicator of T-cell senescence/exhaustion that is associated with biolo

175 d an 85 kb BAC clone, 346J21, that carries a cell senescence gene (SEN16), previously mapped to 16q24

176 have identified a 360 kb YAC that carries a cell senescence gene, SEN16.

177 T-cell senescence has also been identified as an instigato

178 Although the phenotype of T-cell senescence has been extensively investigated, few s

179 intriguing data on the role of caveolin-1 in cell senescence have emerged.

180 evolution of diploid sexual reproduction and cell senescence (i.e., cell aging).

181 Markers of CD4(+) T-cell senescence (ie, the percentage of CD28(-)CD57(+) ce

182 collagen (GC) express hallmarks of premature cell senescence, ie, increase in the proportion of cells

183 tic subunit plays an important role in human cell senescence, immortalization, and carcinogenesis.

184 ong bone, and that inhibition of endothelial cell senescence improves GC-impaired bone angiogenesis w

185 This suggests that IR induces hematopoietic cell senescence in a p53-p21(Cip1/Waf1)-dependent manner

186 T-cell senescence in cases was independently associated wi

187 ether, our data suggest that prevention of T cell senescence in Fas-Tg mice may be a factor in induct

188 the average length of telomeres and leads to cell senescence in HeLa cells and cell death in HeLa, U2

189 These findings identify a premature T-cell senescence in ICL that might be caused by chronic T

190 Cancer cell senescence in lung squamous cell carcinoma (LUSC) i

191 These effects were due to massive cell senescence in mammary tissue, which was associated

192 in mammary epithelium induces premature stem cell senescence in mammary transplants and decreases mam

193 t in young mice induces vascular endothelial cell senescence in metaphysis of long bone, and that inh

194 indings suggest a role for Abeta-induced OPC cell senescence in neuroinflammation and cognitive defic

195 ll proliferation and apoptosis and inhibited cell senescence in normal VSMCs.

196 ted exacerbation of telomere dysfunction and cell senescence in the absence of any other genetic or e

197 n fibroblasts will better define the role of cell senescence in the aging process and in tumorigenesi

198 ein, we have investigated the role of immune cell senescence in the response to checkpoint inhibitors

199 ally, inhibition of ROS production mitigated cell senescence in these cells.

200 y vessels of strategies aimed at controlling cell senescence in various contexts.

201 effector T cells averted the tEV-mediated T cell senescence in vitro and in vivo in cell adoptive tr

202 aired the autophagic flux and induced cancer cell senescence in vitro and in xenograft models.

203 ffector T cell lipid metabolism, prevented T cell senescence in vitro, and enhanced antitumor immunit

204 We describe a stochastic network model of cell senescence in which a primary role is played by tel

205 omes, including episomes such as ERCs, cause cell senescence in yeast.

206 ll migration and invasion and suppression of cell senescence independent of TAp63 and/or TP53 gene st

207 We hypothesized that cell senescence induced by Nutlin-3a exerted therapeutic

208 Ezh2 maintains the repression of key cell senescence inducer genes through H3K27me3, and dele

209 Cell senescence induces the expression of miR-1204 throu

210 s originally identified in studies to reveal cell senescence-inducing factors.

211 permanent and irreversible growth arrest of cell senescence is a central paradigm of aging.

212 Cell senescence is a physiological program of terminal g

213 Cell senescence is a process of irreversible arrest of c

214 Cell senescence is an important tumour suppressor mechan

215 Here, we show that cell senescence is an intrinsic part of the developmenta

216 Cell senescence is broadly defined as the physiological

217 two-photon probe (AHGa) for the detection of cell senescence is designed.

218 BM microenvironment and that the BM stromal cell senescence is driven by p16INK4a expression.

219 This satellite cell senescence is due to accumulation of the SUMO ligas

220 Also, cell senescence is found to be useful in the maintenance

221 etabolic profile of the complex landscape of cell senescence is needed.

222 T cell senescence is thought to contribute to immune funct

223 In the nonobese diabetic mouse model, beta-cell senescence largely depended on damage inflicted by

224 to be involved in a tissue-specific form of cell senescence, leading to the differentiation of kerat

225 port a new human genetic disease that causes cell senescence, liver and immune dysfunction, and early

226 ), whereas EX increased the hepatic stellate cell senescence marker CCN1 (P < 0.01 vs. O-SED).

227 tivation was strongly associated with the NK cell senescence marker CD57, arguing for the need for se

228 Cell senescence may be an important factor in chronic re

229 tors is important because induction of tumor cell senescence may represent a therapeutic approach for

230 CDKN2A expression (a cell senescence mediator) was measured in peripheral blo

231 l cells, thus expanding our insight into the cell senescence molecular machinery.

232 Premature T-cell senescence occurs not only in RA, but also has been

233 CECs as mirror cells for in vivo endothelial cell senescence, of particular interest in the context o

234 n that critically short telomeres can induce cell senescence or apoptosis.

235 cytomegalovirus (CMV) are thought to drive T-cell senescence, other microbes may be important for the

236 We evaluated three mechanisms leading to cell senescence: oxidative stress, DNA damage, and repli

237 These cells showed accelerated cell senescence pathway accompanied by increased inflamm

238 The cell senescence pathway also showed sexual dimorphism.

239 SPI-fed rat serum inhibited the osteoblastic cell senescence pathway.

240 veolin-1 expression to suppress osteoblastic cell senescence pathways.

241 mergence of a p21-dependent, p53-independent cell senescence phenotype.

242 igger not only beta-cell death but also beta-cell senescence, potentially via cytokine-dependent mech

243 BRCA1) in cell cycle arrest, DNA damage, and cell senescence, preventing maladaptive repair.

244 amming process via significantly influencing cell senescence, proliferation and chromatin structure.

245 Tumor cell senescence promoted an anti-tumor immune response b

246 progerin production during the induction of cell senescence, providing mechanistic insight into how

247 atory genes, with negative enrichment of the cell senescence-related regulators, compared to the posi

248 and pro-anabolic effects, its impact on IVD cell senescence remains elusive.

249 Although MLN4924-induced cell senescence seems to be dependent on induction of p5

250 entified the role of sirtuin 1 in preventing cell senescence; shed light on the role of polycomb grou

251 ysis of the senescent phenotype identified a cell senescence signature distinct for CEnC.

252 tors to late graft loss; features of tubular cell senescence, such as increased p16(INK4a) expression

253 y offer an efficient way for intervention on cell senescence thanks to their unique capacity to degra

254 ermore, our data match a simple model of red cell senescence that assumes both an age-dependent destr

255 re likely plays a checkpoint function during cell senescence that underscores its selective role as a

256 activation, and potently induce endothelial cell senescence that was recapitulated in vivo in microv

257 gulates diverse signaling pathways involving cell senescence, the cell cycle, and apoptosis.

258 The main conclusion is that, without cell senescence, the evolutionary advantages of sexual r

259 Although p16 may be involved in cell senescence, the physiologic role of p16 is still un

260 s p53 (also known as TRP53)-dependent cancer cell senescence, thereby increasing tumorigenic potentia

261 is the signature marker for age-associated T-cell senescence, these findings provide novel mechanisti

262 that Rac1 activity serves as a regulator of cell senescence through modulation of cellular ROS, geno

263 stress can induce retinal pigment epithelial cell senescence through p53-p21(Cip1/WAF1)-Rb pathway.

264 continuously eliminated, can rapidly induce cell senescence through signaling pathways very similar

265 Human beta-cell senescence thus involves chromatin-driven upregulat

266 rovide the first in vivo evidence that links cell senescence to aging due to impaired function of Brc

267 We reported T-cell senescence to be similar in people living with HIV

268 -dependent macrophage activation and tubular cell senescence to delay renal fibrosis.

269 llow repair to occur or trigger apoptosis or cell senescence to prevent propagation of damaged DNA.

270 programming efficiency which may result from cell senescence trigged by up-regulated Ink4a/Arf locus.

271 A novel mouse model of conditional AT2 cell senescence was generated to study the role of cellu

272 present studies the possible involvement of cell senescence was investigated.

273 Cervical cancer cell senescence was partially overcome by DEK overexpres

274 The degree of adipose cell senescence was positively correlated with whole-bod

275 eral other changes that have been related to cell senescence were observed: these included markers of

276 to chromatin are thought to be essential to cell senescence, which is key to tumorigenesis and aging

277 elicobacter infection, possibly because of T-cell senescence, which may indirectly protect against th

278 ostate leads to hyperplasia and also induces cell senescence, which may, in turn, function as a barri

279 d with SARS-CoV-2 and CMV have accelerated T cell senescence, which might lead to an increased risk o

280 E6/E7 had an additive effect on constraining cell senescence while promoting cell proliferation and i

281 B2-driven mammary carcinomas triggered tumor cell senescence, without compromising the animals' healt