ライフサイエンスコーパス: cellular senescence

1 g the chronic infection phase, likely due to cellular senescence.

2 rotects mouse and rat cells from ROS-induced cellular senescence.

3 I diminished their proliferation and induced cellular senescence.

4 ng many of the abnormalities associated with cellular senescence.

5 to-mesenchymal transition, angiogenesis, and cellular senescence.

6 ilure to reabsorb the primary cilium induces cellular senescence.

7 transcriptional activity, growth arrest, and cellular senescence.

8 d breaks (DSBs), G0/G1 cell cycle arrest and cellular senescence.

9 d tumor-suppressor functions, which includes cellular senescence.

10 s reveal new insights and gene regulators of cellular senescence.

11 l regenerative capacity because of increased cellular senescence.

12 changes affect specific genes that regulate cellular senescence.

13 e ends of chromosomes, eventually triggering cellular senescence.

14 ers cell development, and induces a state of cellular senescence.

15 t (KO) of YAP in hMSCs resulted in premature cellular senescence.

16 ein, in replication- and doxorubicin-induced cellular senescence.

17 owever, it is unknown if Pak2 contributes to cellular senescence.

18 ursors, mitophagy inducers and inhibitors of cellular senescence.

19 ondrial proteins were involved in regulating cellular senescence.

20 aying the onset of CDKN2a/p16(INK4a) -driven cellular senescence.

21 regulators of splicing factor expression in cellular senescence.

22 -renewal, control of cellular quiescence and cellular senescence.

23 ely impaired EGFR signaling and the onset of cellular senescence.

24 , reduced DNA repair responses, and elevated cellular senescence.

25 t E6/E7 inhibition phenotypically results in cellular senescence.

26 by encouraging proliferation and inhibiting cellular senescence.

27 ase genes and permanent cell cycle arrest or cellular senescence.

28 amage response, and consequently attenuating cellular senescence.

29 feration, whereas in old females it leads to cellular senescence.

30 BRAF(V600E)-induced ERK hyperactivation and cellular senescence.

31 such as TGF-beta, cigarette smoke (CS), and cellular senescence.

32 vival after ionizing radiation, and prevents cellular senescence.

33 g skin fibroblast proliferation and delaying cellular senescence.

34 y adversity and telomere length, a marker of cellular senescence.

35 TS) patients compared with natural aging and cellular senescence.

36 al inhibition of LSD1 triggers G1 arrest and cellular senescence.

37 on maintained in the context of p53-mediated cellular senescence.

38 cell viability and was sufficient to trigger cellular senescence.

39 ive DNA damage triggers telomere erosion and cellular senescence.

40 n vitro and in vivo despite the induction of cellular senescence.

41 ion in various cellular processes, including cellular senescence.

42 at their loss leads to cell-cycle arrest and cellular senescence.

43 we show the critical role of mitochondria in cellular senescence.

44 veal the mechanism by which OGT functions in cellular senescence.

45 p16 expression in tumor cells, and promoted cellular senescence.

46 nhances G1 arrest and a phenotype resembling cellular senescence.

47 ) cells more sensitive to paclitaxel-induced cellular senescence.

48 s that autophagy promotes the development of cellular senescence.

49 nt biological function in ROS production and cellular senescence.

50 ly, increased ROS production and accelerated cellular senescence.

51 in the context of macrophage activation and cellular senescence.

52 TGFbeta, DNA-damage-response signalling and cellular senescence.

53 l model executed by MIB1 and WRN to regulate cellular senescence.

54 matory phenotype that can be associated with cellular senescence.

55 Platinum-based chemotherapy induces cellular senescence.

56 n cytosolic DNA sensor that is essential for cellular senescence.

57 ductions in cell proliferation and increased cellular senescence.

58 dergoing morphological changes that resemble cellular senescence.

59 CDK4/6 activity and have important roles in cellular senescence.

60 signaling pathways are enhanced, leading to cellular senescence.

61 V exposure causes cells to prematurely enter cellular senescence.

62 oxidative stress, and activated signaling of cellular senescence.

63 tiated cells that exhibit characteristics of cellular senescence.

64 tion and display transcriptional features of cellular senescence.

65 on, and repair, as well as transcription and cellular senescence.

66 Cellular senescence, a form of stable cell cycle arrest

67 Cellular senescence, a permanent state of replicative ar

68 Cellular senescence, a process driven in part by telomer

69 Cellular senescence, a state of stable cell cycle arrest

70 Cellular senescence, a stress-induced irreversible growt

71 rks of aging, including telomere shortening, cellular senescence, activation of PI3 kinase-mTOR signa

72 tion of MC(1) is a viable strategy to induce cellular senescence, affording a distinct way to control

73 lls is known to cause genome aberrations and cellular senescence, although the molecular basis for th

74 Cellular senescence, an integral component of aging and

75 Cellular senescence, an irreversible growth arrest trigg

76 an alter the tumor microenvironment, causing cellular senescence and activating cancer-promoting infl

77 pression in several aging phenotypes such as cellular senescence and age itself.

78 Here, we review molecular links between cellular senescence and age-associated complications and

79 ink between defective mitochondrial fission, cellular senescence and age-dependent oxidative stress r

80 We define a particular distinction between cellular senescence and ageing and propose that caveolin

81 iew the cellular and molecular links between cellular senescence and aging and discuss the novel ther

82 apt the microenvironment which could lead to cellular senescence and aging.

83 he HER2-AKT1 cascade augments damage-induced cellular senescence and apoptosis, and enhances STING-me

84 oversimplified scenario, p53, an inducer of cellular senescence and apoptosis, may thus unfavorably

85 Aging and death of cells (cellular senescence and apoptosis, respectively), trigge

86 h blocked their tumorigenic capacity through cellular senescence and apoptosis.

87 ds promoted G1 cell cycle arrest followed by cellular senescence and apoptosis.

88 Here we review mechanisms of cellular senescence and approaches to target this pathwa

89 k loop cascade during DDR and contributes to cellular senescence and chemotherapy resistance in ovari

90 nce the progression of colorectal cancer via cellular senescence and death induced by DNA double-stra

91 n renal carcinoma, T1(Pr alphaTACE) triggers cellular senescence and disrupts MMP-mediated proteolysi

92 olar type II cells and club cells, increased cellular senescence and DNA damage, increased fibroblast

93 recombination (HR) DNA repair, resulting in cellular senescence and embryonic lethality in mice.

94 are long-lived, are relatively resistant to cellular senescence and exhaustion, and are capable of s

95 ion inhibition, impaired mineral resorption, cellular senescence and extracellular vesicles that act

96 ons of cellular aging and death (escape from cellular senescence and failed apoptosis of severely dam

97 satively linked to perpetual DSBs signaling, cellular senescence and fibrosis.

98 stress-induced DNA damage and mutagenesis in cellular senescence and immortalization, here we profile

99 pathways, DNA repair, chromatin remodelling, cellular senescence and immune cell function.

100 MicroRNA-570 is a novel regulator of cellular senescence and inflammaging.

101 later response is associated with increased cellular senescence and inhibition of transcriptional co

102 also involved in reduction of sirtuin-1 and cellular senescence and is activated by p38 mitogen-acti

103 tumor-infiltrating lymphocytes (TIL) induces cellular senescence and limits tumor suppression.

104 T1 downregulation released the repression of cellular senescence and migration activity in SK-N-SH ce

105 trate that Pak2 is an important regulator of cellular senescence and organismal aging, in part throug

106 ng DNA damage, HOTAIR has a critical role in cellular senescence and platinum sensitivity.

107 SIN3B was required for PTEN-induced cellular senescence and prevented progression to invasiv

108 required for expression of genes involved in cellular senescence and regulated the deposition of newl

109 at MIB1-mediated degradation of WRN promotes cellular senescence and reveal a novel model executed by

110 These cells possessed characteristics of cellular senescence and showed a strong activation of Sp

111 with Atm deletion leads to the overcoming of cellular senescence and the development of CLL-like dise

112 an unexpected function of telomerase during cellular senescence and tumorigenesis.

113 link between aberrant chromatin remodeling, cellular senescence, and accelerated aging.

114 benchmark resource for researchers to study cellular senescence, and our systems biology analyses re

115 AKT pathways on splicing factor expression, cellular senescence, and proliferation kinetics in senes

116 ession preserved telomere integrity, delayed cellular senescence, and reduced inflammatory cytokine e

117 tosidase (SA-beta-Gal) activity, a marker of cellular senescence; and elevated levels of phosphorylat

118 n, for example, by differentially regulating cellular senescence, apoptosis, and other p53-mediated b

119 consequent onset of telomeric DNA damage and cellular senescence are a general determinant of species

120 Indeed, pathological conditions such as cellular senescence are accompanied by changes in cell d

121 Loss of proteostasis and cellular senescence are key hallmarks of aging, but dire

122 Aging and cellular senescence are known contributors to the pathop

123 ack of evidence, it is not possible to label cellular senescence as a cause or a consequence of neuro

124 etory phenotype, and provides an overview of cellular senescence as an emerging opportunity to interv

125 salivary function was closely accompanied by cellular senescence, as evidenced by a persistent DNA da

126 impaired antiprotease defenses, DNA damage, cellular senescence, autoantibody generation, and cortic

127 t microbial infections, anti-tumor immunity, cellular senescence, autophagy, and autoimmune and infla

128 confirmed that DLX3 mutation (Q178R) delayed cellular senescence, but also prevented aging-mediated b

129 vate DDR signaling, genomic instability, and cellular senescence, but the links among these events re

130 of AURKA, causes primary cilia formation and cellular senescence by irreversibly arresting cell growt

131 We found that MDM2 can promote cellular senescence by modulating WRN stability.

132 ces ovarian cancer growth while antagonizing cellular senescence by repressing the expression of cycl

133 , which is increased in COPD cells, reverses cellular senescence by restoring the antiaging molecule

134 Cellular senescence can also be a controlled programme o

135 Cellular senescence can be broadly defined as a stable,

136 cells in the skin and how the persistence of cellular senescence can promote impaired regenerative ca

137 ine in bone healing and identified increased cellular senescence caused by a systemic and local proin

138 Cellular senescence causes a proinflammatory cellular ph

139 , SYNPO2L), protein homoeostasis (BAG3), and cellular senescence (CDKN1A).

140 ific aspects of the aging process, including cellular senescence, chronic inflammation, and the age-d

141 by UVB diminished G1 arrest, DNA repair, and cellular senescence coincident with enhanced cell death

142 Cellular senescence contributes to age-related tissue dy

143 Based on these data, we conclude that cellular senescence contributes to altered progenitor ce

144 Because cellular senescence contributes to renal aging and promo

145 Cellular senescence defines an irreversible cell growth

146 y of SOCS1 to interact with p53 and regulate cellular senescence depends on a structural motif that i

147 in early pubertal mice results in premature cellular senescence, depleted MSPCs pool, and impaired o

148 ) results in a number of cellular responses (cellular senescence, deregulated nutrient sensing and de

149 of proteostasis, mitochondrial dysfunction, cellular senescence, deregulated nutrient sensing, stem

150 onatal NC cells, but showed limited signs of cellular senescence despite the advanced age of the dono

151 Additionally, enhanced cellular senescence, determined by senescence-associated

152 19) reports that during ageing of the heart, cellular senescence develops independently of telomere l

153 Our study demonstrates that cellular senescence drives hepatic steatosis and elimina

154 ression, which can potentially contribute to cellular senescence during aging.

155 eration, but also increased inflammation and cellular senescence during aging.

156 ned with cell proliferation (e.g. Scn4b) and cellular senescence (e.g. Cdkn2a products) responses.

157 Cellular senescence entails an irreversible growth arres

158 w discusses the mechanisms and modulators of cellular senescence establishment and induction of a sen

159 However, mTert (-/-) cells approached cellular senescence faster and exhibited a significantly

160 Cellular senescence, first described in vitro in 1961, h

161 Furthermore, cellular senescence genes are strongly conserved in mamm

162 Expression of cellular senescence genes in PPMS NPCs was found to be r

163 a very heterogeneous disease, resulting from cellular senescence, genetic predisposition and environm

164 Furthermore, we highlight the evidence that cellular senescence has a causative role in multiple dis

165 Studying the phenomenon of cellular senescence has been hindered by the lack of sen

166 Cellular senescence has been shown to contribute to skin

167 Cellular senescence has emerged as a potent tumor suppre

168 In recent years, cellular senescence has generated a lot of interest amon

169 In this context, cellular senescence has received considerable attention

170 as a stress response end point, the view of cellular senescence has since evolved into one encompass

171 er the past 20 years, various identifiers of cellular senescence have been used to quantify the abund

172 ole for skeletal muscle lamin A/C to prevent cellular senescence, IL-6 expression, hyperosteoclastoge

173 liver that may contribute to or derive from cellular senescence, implying that the latter may be bot

174 RSV induced S-phase arrest and cellular senescence in a dose-dependent manner in U2OS a

175 Finally, we focus on the role of cellular senescence in a number of endocrine diseases, i

176 r is tempered by the activation of premature cellular senescence in an NF1-deficient background.

177 ingly, overexpression of caveolin-1 restores cellular senescence in both A549 and H460 lung cancer ce

178 lication and oxidative stresses in mediating cellular senescence in cancer cells treated with RSV.

179 The role of cellular senescence in development of vascular aging phe

180 hibitory effects on oxidative stress-induced cellular senescence in endothelial cells and skin fibrob

181 accelerated aging to investigate the role of cellular senescence in HFpEF development.

182 Loss of WRN function induces cellular senescence in human cancer cells.

183 cells (GMSC-EVs) on oxidative stress-induced cellular senescence in human endothelial cells and skin

184 rize the current literature on the impact of cellular senescence in NAFLD/NASH and discuss the effect

185 cells interpret signals that normally induce cellular senescence in non-regenerating mammals (Mus and

186 to unappreciated role for CXCR2 in mediating cellular senescence in pathological wound repair.

187 We report that SATB1 prevents cellular senescence in post-mitotic dopaminergic neurons

188 on of the HIRA S231A mutant delays premature cellular senescence in primary human fibroblasts, wherea

189 Telomere shortening induces cellular senescence in proliferative cells.

190 dings reveal a novel role for p16(Ink4a) and cellular senescence in promoting insulin secretion by be

191 mune signaling, but also prevented premature cellular senescence in response to dysfunctional telomer

192 ) plays a tumor suppressive role by inducing cellular senescence in response to oncogenic stress.

193 We observed phenotypes that are central to cellular senescence in SATB1 knockout dopamine neurons i

194 Considerable evidence implicates cellular senescence in the biology of aging and chronic

195 This Review examines cellular senescence in the context of ageing and AD, and

196 ion of oncogenic K-Ras (K-Ras(G12D)) induces cellular senescence in the lung of wildtype but not cave

197 edge of both the drivers and consequences of cellular senescence in tissues and organs remains limite

198 bociclib enhances G(1) cell cycle arrest and cellular senescence in tumour cells.

199 P attenuates cancer cell growth by promoting cellular senescence in vivo, which correlates with resto

200 em, completing genome replication to prevent cellular senescence in yeast, humans, and most other euk

201 Further analysis revealed the induction of cellular senescence in zebrafish embryos overexpressing

202 uppression of primary cilia formation limits cellular senescence induced by alisertib.

203 cells against mitochondrial dysfunction and cellular senescence induced by oxidative stress.

204 luence cell fate as they regulate autophagy, cellular senescence, inflammation, bioenergetic metaboli

205 HK1S345 phosphorylation and thereby prevents cellular senescence, IPF and carcinoma formation.

206 Cellular senescence is a candidate mechanism that might

207 Cellular senescence is a cell state implicated in variou

208 Cellular senescence is a cell-intrinsic response to DNA

209 Cellular senescence is a contributor to intervertebral d

210 Cellular senescence is a driver of various aging-associa

211 Cellular senescence is a form of adaptive cellular physi

212 Collectively, these results indicate that cellular senescence is a fundamental mechanism driving r

213 Cellular senescence is a major driver of age-related dis

214 Cellular senescence is a mechanism by which cells perman

215 Cellular senescence is a mechanism used by mitotic cells

216 Cellular senescence is a permanent growth arrest in cell

217 In this article we hypothesize that cellular senescence is a phenotype that results from the

218 Cellular senescence is a phenotypic state that contribut

219 Cellular senescence is a potent tumor suppressor mechani

220 Cellular senescence is a primary aging process and tumor

221 Cellular senescence is a process of cellular growth arre

222 Cellular senescence is a stable cell growth arrest that

223 Cellular senescence is a stable growth arrest that is im

224 Cellular senescence is a state of irreversibly arrested

225 Cellular senescence is a stress response that elicits a

226 Cellular senescence is a stress-responsive cell-cycle ar

227 Cellular senescence is a terminal cell cycle arrested st

228 Cellular senescence is an antiproliferative response wit

229 the completion of mitosis in cells in which cellular senescence is caused by the inhibition of AURKA

230 Cellular senescence is characterized by a permanent cell

231 Cellular senescence is characterized by stable cell-cycl

232 Cellular senescence is due to replicative and stress-rel

233 In addition, CPT-induced cellular senescence is facilitated by the expression of

234 Detection of cellular senescence is important not only in the study o

235 Cellular senescence is now considered an important drivi

236 Cellular senescence is physiologically beneficial in sev

237 Osteoarthritis is an age-related disease and cellular senescence is predicted to be a significant com

238 and primary cilia formation is enhanced when cellular senescence is promoted by other senescence-indu

239 water content as a widespread concomitant of cellular senescence is reviewed.

240 Cellular senescence is thought to contribute to age-asso

241 Despite its popularity, cellular senescence is weakly defined and is frequently

242 ssociated organ fibrosis, marked by elevated cellular senescence, is a growing health concern.

243 growth restriction, including the evasion of cellular senescence, is a hallmark of cancer.

244 Here we show that during cellular senescence, L1 (also known as LINE-1) retrotran

245 Ageing is characterised by cellular senescence, leading to imbalanced tissue mainte

246 r mechanistic studies reveal an elevation of cellular senescence marked by senescence-associated beta

247 Cellular senescence markers are detectable within IPF lu

248 regulation of splicing factor expression and cellular senescence may derive in part from altered acti

249 rate organogenesis and support the view that cellular senescence may have arisen in evolution as a de

250 Understanding the mechanisms of cellular senescence may result in new treatments for chr

251 le in various biological processes including cellular senescence, metabolism, and inflammatory respon

252 DNA damage and discuss their interplay with cellular senescence, mitotic catastrophe, and autophagy.

253 Cellular senescence occurs by proliferative exhaustion (

254 terized by a permanent proliferation arrest, cellular senescence occurs in response to endogenous and

255 and clearance, cell growth retardation, and cellular senescence of DC fibroblasts.

256 ological treatment with quercetin alleviated cellular senescence of dermal fibroblasts.

257 d AD, and discusses which of the processes - cellular senescence or AD - might come first.

258 perience replication stress that can lead to cellular senescence or apoptosis.

259 ature aging is not associated with increased cellular senescence or telomere length but is a result o

260 that drive a permanent proliferative arrest (cellular senescence) or regulated cell death.

261 mor-suppressor genes, while genes inhibiting cellular senescence overlap with pro-longevity and oncog

262 repression under hypoxia does not result in cellular senescence, owing to hypoxia-associated impaire

263 restores sirtuin-1 and suppresses markers of cellular senescence (p16(INK4a), p21(Waf1), and p27(Kip1

264 n mechanism that initiates and maintains the cellular senescence phenotype.

265 cell load, and partial reversal of multiple cellular senescence phenotypes in a dose-dependent manne

266 Cellular senescence plays a critical role in tumorigenes

267 oxidative stress and inflammation, but also cellular senescence processes, may contribute to age-rel

268 We also build cellular senescence protein-protein interaction and co-e

269 in human tumors, as a critical repressor of cellular senescence, providing a novel connection betwee

270 Cellular senescence refers to a state of irreversible ce

271 gical parameters also reveal novel potential cellular senescence regulators.

272 ss-induced upregulation in the expression of cellular senescence-related genes, such as beta-galactos

273 itically short telomeres, a major trigger of cellular senescence, remains unknown.

274 Reprogramming of cellular senescence signaling by SPI-associated isoflavo

275 Genes inducing cellular senescence tend to be overexpressed with age in

276 ion to a critically short length can lead to cellular senescence that irreversibly prevents cells fro

277 ong others - can engender a state of chronic cellular senescence that is characterized by the secreti

278 ses identify several candidate biomarkers of cellular senescence that overlap with aging markers in h

279 iological systems, such as nutrient sensing, cellular senescence, the systemic environment and the gu

280 veal an unexpected role of MDM2 in promoting cellular senescence through a p53-independent manner.

281 igenesis by overcoming the PTEN loss-induced cellular senescence through inhibition of p21 activation

282 ocular GVHD pathogenesis and stress-induced cellular senescence through the senescence-associated se

283 The activation of cellular senescence throughout the lifespan promotes tum

284 The contribution of cellular senescence to neurodegeneration is still unclea

285 a therapeutic target by exerting effects on cellular senescence to retard HCC progression.

286 Loss of SATB1 causes activation of a cellular senescence transcriptional program in dopamine

287 positively associated with the induction of cellular senescence, verified by senescence-associated b

288 ll line HTR8/SVneo induced growth arrest and cellular senescence via activation of p38-mitogen-activa

289 DUSP3, which regulates cellular senescence, was identified as one of the diseas

290 nesis, apoptosis, cell cycle regulation, and cellular senescence were affected by targeting SYK.

291 of cell proliferation, colony formation, and cellular senescence were evaluated in human HCC cell lin

292 n, we report that expression of hallmarks of cellular senescence were identified in SOX2(+) progenito

293 ons (c.533 A>G and c.571_574delGGGG) delayed cellular senescence when they were introduced into pre-o

294 of mitochondrial dynamics has been linked to cellular senescence, which contributes to advanced age-r

295 Aging is associated with increased cellular senescence, which is hypothesized to drive the

296 es, in oncogene addiction, and in overcoming cellular senescence, which suggests calcineurin-NFAT sig

297 ge disrupted genomic integrity and triggered cellular senescence, which was accompanied by tumor-prom

298 migrate on the collagen fibrils and undergo cellular senescence, while MCF-7 do not exhibit these be

299 likely to create a positive feedback loop of cellular senescence within the adipocyte precursor compa

300 Many genes play a role in cellular senescence, yet a comprehensive understanding o