ライフサイエンスコーパス: senescence

1 e due to random environmental fluctuations ("senescence").

2 cell-autonomous process of 'oncogene-induced senescence'.

3 ugh recognizing cytoplasmic chromatin during senescence.

4 CPK1 phosphorylation hotspot, promote early senescence.

5 different cell biology and disease models of senescence.

6 food, and could be achieved by delaying crop senescence.

7 g pathways are enhanced, leading to cellular senescence.

8 ontext of macrophage activation and cellular senescence.

9 lasmic chromatin recognition and SASP during senescence.

10 es modestly in early aging and sharply after senescence.

11 DNA-damage-response signalling and cellular senescence.

12 membrane potential leading to cell death or senescence.

13 romoter sequence motifs associated with leaf senescence.

14 xecuted by MIB1 and WRN to regulate cellular senescence.

15 mechanisms such as cell cycle regulation and senescence.

16 enotype that can be associated with cellular senescence.

17 tion of retinoblastoma (RB) protein-mediated senescence.

18 potential consequences for the evolution of senescence.

19 onic infection phase, likely due to cellular senescence.

20 Platinum-based chemotherapy induces cellular senescence.

21 ic DNA sensor that is essential for cellular senescence.

22 A damage and p53-dependent apoptosis, but no senescence.

23 ing in plant immunity and developmental leaf senescence.

24 ding the plant's defense response, to nodule senescence.

25 ced cell death, myofibroblast formation, and senescence.

26 rmation akin to that of cells in replicative senescence.

27 in cell proliferation and increased cellular senescence.

28 morphological changes that resemble cellular senescence.

29 ctivity and have important roles in cellular senescence.

30 bule stabilizing agent and potent inducer of senescence.

31 r a reduced level of AS activity during leaf senescence.

32 ge, and activated p38 MAPK, both inducers of senescence.

33 s, cell cycle arrest, DNA damage repair, and senescence.

34 ll-autonomous, 'oncogene-induced' program of senescence.

35 alterations induce p15/16 growth arrest and senescence.

36 shoot branching, root development, and leaf senescence.

37 amics and vascular smooth muscle cell (VSMC) senescence.

38 ass loss, and, consequently, retarding their senescence.

39 ns during nodule formation, development, and senescence.

40 new insights and gene regulators of cellular senescence.

41 chromosomes, eventually triggering cellular senescence.

42 porting symbiosis, and the control of nodule senescence.

43 ents, as well as the timing of flowering and senescence.

44 ear antigens also repress CDKN2A to suppress senescence.

45 DNA damage response that signals replicative senescence.

46 ontinuous passaging induced replicative cell senescence.

47 pe was not caused by cell death induction or senescence.

48 h-resolution topographical images of cuticle senescence.

49 pressor, which induces cell-cycle arrest and senescence.

50 circumvents destructive, stress-induced cell senescence.

51 Cellular senescence, a permanent state of replicative arrest in o

52 the fitness consequences of maternal effect senescence across species with diverse aging and fertili

53 C(1) is a viable strategy to induce cellular senescence, affording a distinct way to control joint in

54 including soluble factors in the context of senescence, ageing, and age-related diseases.

55 mitochondrial homeostasis could lead to cell senescence, although the underlying mechanism remains un

56 e differences in DNA damage and induction of senescence among cells of colonies.

57 TPA promotes skin carcinogenesis by inducing senescence and a SASP.

58 trate that persistent DNA damage potentiates senescence and activates cytokine signaling.

59 , we review molecular links between cellular senescence and age-associated complications and highligh

60 e function and discuss their implications in senescence and age-related diseases.

61 icroenvironment which could lead to cellular senescence and aging.

62 ion, even at low dose-rates, can induce cell senescence and alter gene expression via a hitherto unch

63 however, only canonical p53 functions (i.e. senescence and apoptosis) are attributed to inflammation

64 lified scenario, p53, an inducer of cellular senescence and apoptosis, may thus unfavorably contribut

65 Aging and death of cells (cellular senescence and apoptosis, respectively), triggered by or

66 Here we review mechanisms of cellular senescence and approaches to target this pathway therape

67 bolism; however, its role in regulating VSMC senescence and atherosclerosis is unclear.

68 important and unrecognized inhibitor of VSMC senescence and atherosclerosis.

69 ghts into the dual roles of tumor-associated senescence and can potentially impact the treatment of p

70 that genotoxic stress and ensuing placental senescence and cytokine production could represent a bro

71 : quiescence, ignorance, anergy, exhaustion, senescence and death.

72 II cells and club cells, increased cellular senescence and DNA damage, increased fibroblast activati

73 ation (HR) DNA repair, resulting in cellular senescence and embryonic lethality in mice.

74 Immune senescence and exhaustion paradigms offer only partial e

75 otype, while another subpopulation undergoes senescence and growth arrest.

76 duced DNA damage and mutagenesis in cellular senescence and immortalization, here we profiled spontan

77 the transition from primary culture through senescence and immortalization.

78 regulation of mammalian SIRT1 protein during senescence and in vivo ageing.

79 mice had reduced atherosclerosis, markers of senescence and inflammation compared with littermate con

80 ) in tert mutants exhibited higher levels of senescence and inflammation.

81 ion invokes a proliferation defect, triggers senescence and inhibits colony formation in liver, but a

82 thway that initiates formation of CCF during senescence and is a potential target for drug-based inte

83 phytosulfokine alpha (PSKalpha) for delaying senescence and lessening decay in strawberry fruits duri

84 iltrating lymphocytes (TIL) induces cellular senescence and limits tumor suppression.

85 receptor (NK1R) axis triggers biliary damage/senescence and liver fibrosis in bile duct ligated and M

86 pregulation of several genes associated with senescence and malignancy, including SERPINE1.

87 ent and demonstrates that tumor cells induce senescence and metabolic changes in adipocytes, potentia

88 ism underlying the link between muscle aging/senescence and osteoporosis.

89 ce lacking Klf5 in VSMCs exacerbate vascular senescence and progression of angiotensin II (Ang II)-in

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

91 ediated degradation of WRN promotes cellular senescence and reveal a novel model executed by MIB1 and

92 S and OIS and discover determinants of acute senescence and SAHF formation.

93 rface protein that is broadly induced during senescence and show that uPAR-specific CAR T cells effic

94 However, at what tumor stage and how senescence and the SASP act on endogenous tumor growth i

95 genome profiles during oncogenic RAS-induced senescence and validating central findings in different

96 age (reactive oxygen species, apoptosis, and senescence) and endothelial repair (cell proliferation a

97 lated declines in reproduction (reproductive senescence) and survival (actuarial senescence) in most

98 d ductular reaction, liver fibrosis, biliary senescence, and biliary inflammation were observed in NK

99 rrant gene regulation, stem cell exhaustion, senescence, and deregulated cell/tissue homeostasis.

100 d, and liver damage, changes in biliary mass/senescence, and inflammation as well as liver fibrosis w

101 Fibrosis, Shc expression, markers of senescence, and nicotinamide adenine dinucleotide phosph

102 k resource for researchers to study cellular senescence, and our systems biology analyses reveal new

103 ays critical roles in adaptation, evolution, senescence, and tumorigenesis.

104 altered organellar structures and increased senescence- and pathogenesis-related gene expression.

105 ntrahepatic bile duct mass, inflammation and senescence; and fibrosis, angiogenesis, and cAMP/phospho

106 ample, by differentially regulating cellular senescence, apoptosis, and other p53-mediated biological

107 ed, pathological conditions such as cellular senescence are accompanied by changes in cell density.

108 Apoptosis and senescence are the two major outcomes upon irreversible

109 idence, it is not possible to label cellular senescence as a cause or a consequence of neurodegenerat

110 These findings identify chemotherapy-induced senescence as a culprit behind tumor promotion, suggesti

111 ORE1), the developmental master regulator of senescence, as a direct CPK1 phosphorylation substrate.

112 n elevation of cellular senescence marked by senescence-associated beta-galactosidase (SA-beta-gal),

113 ease of cell doubling and a 39% reduction in senescence-associated beta-galactosidase activity (p < 0

114 A higher prevalence of cells positive for senescence-associated beta-galactosidase activity was al

115 nce was determined by immunofluorescence and senescence-associated beta-galactosidase staining.

116 it increases hallmarks of senescence such as senescence-associated beta-galactosidase, increased p21

117 hesis in the production of cisplatin-induced senescence-associated cancer stem cells, as well as tumo

118 However, therapeutic approaches targeting senescence-associated CSCs remain to be explored.

119 utic strategy by suppressing therapy-induced senescence-associated CSCs.

120 eutic potential of senolytic CAR T cells for senescence-associated diseases.

121 Increased senescence-associated distension of satellites (SADS) an

122 af senescence is driven by the expression of senescence-associated genes (SAGs).

123 are transcription-dependent and enriched for senescence-associated genes, exemplified by IL1B, where

124 We identify senescence-associated heterochromatin domains (SAHDs).

125 r-SAHD interactions lead to the formation of senescence-associated heterochromatin foci (SAHFs) in OI

126 Our results show that metformin reshapes the senescence-associated miRNA/isomiR patterns of endotheli

127 12 muscle cells, and the p16Ink4a may induce senescence-associated secretory phenotype (SASP) and IL-

128 th increased levels of senescent markers and senescence-associated secretory phenotype (SASP) compone

129 ns were used to characterize the age-related senescence-associated secretory phenotype (SASP) gene ex

130 The senescence-associated secretory phenotype (SASP) has rec

131 Mechanistically, TIMP1 loss reprograms the senescence-associated secretory phenotype (SASP) of sene

132 cGAS promotes inflammatory senescence-associated secretory phenotype (SASP) through

133 rrest, apoptosis resistance, production of a senescence-associated secretory phenotype (SASP), mitoch

134 and growth-stimulatory molecules, termed the senescence-associated secretory phenotype (SASP), which

135 of a bioactive secretome, referred to as the senescence-associated secretory phenotype (SASP).

136 omplex proinflammatory secretome, termed the senescence-associated secretory phenotype (SASP).

137 at kill senescent cells or inhibitors of the senescence-associated secretory phenotype (SASP).

138 ress-induced cellular senescence through the senescence-associated secretory phenotype (SASP).

139 asts within the aged dentate gyrus display a senescence-associated secretory phenotype and reinforce

140 ctivation, the subsequent development of the senescence-associated secretory phenotype and tumour pro

141 clusion that the elevated DNA damage and the senescence-associated secretory phenotype are preferenti

142 ch in skeletal muscle coincided with reduced senescence-associated secretory phenotype complexity.

143 The activation of the senescence-associated secretory phenotype fuels further

144 hepatic stellate cells (HSCs), exhibiting a senescence-associated secretory phenotype.

145 ammation and extracellular matrix as well as senescence-associated secretory proteins.

146 They find that loss of SIRT1 activity drives senescence-associated sEV release, and treatment with a

147 of several stages of growth from seedling to senescence at hourly intervals.

148 ence of molecular mechanisms underlying leaf senescence between annual and perennial species.

149 tive association of kidney diseases and cell senescence, both culminating in progressive deterioratio

150 chment of underlying kidney disease and cell senescence bring about the conclusion that both entities

151 y life should be associated with accelerated senescence, but empirical tests have yielded mixed resul

152 pathways responsible for induction of T cell senescence by malignant tumors, and then discuss potenti

153 ar pathways associated with the induction of senescence by this protein.

154 nsights into the role of oxidative stress in senescence bypass and immortalization.

155 and reach the effector stage, exhaustion and senescence can limit excessive inflammation and prevent

156 the skin and how the persistence of cellular senescence can promote impaired regenerative capacity, c

157 ), protein homoeostasis (BAG3), and cellular senescence (CDKN1A).

158 esized that alveolar bone osteocytes develop senescence characteristics in old age.

159 mechanisms and regulatory networks defining senescence competence, induction and maintenance remain

160 omatin, transcription factor recruitment and senescence competence.

161 A better understanding of how senescence contributes to joint dysfunction may enhance

162 of non-muscle-specific genes and p16INK4a, a senescence driver encoded in the Cdkn2a locus.

163 but also increased inflammation and cellular senescence during aging.

164 cell proliferation (e.g. Scn4b) and cellular senescence (e.g. Cdkn2a products) responses.

165 on into adipocyte precursors (AP), premature senescence emerged, impairing later stages of adipogenes

166 Cellular senescence entails an irreversible growth arrest that ev

167 ers on CD8 + T cells, an indicator of T-cell senescence/exhaustion that is associated with biological

168 ding the deliberate therapeutic targeting of senescence for health benefits.

169 mplications for understanding the origins of senescence, frailty, and morbidity.

170 Furthermore, cellular senescence genes are strongly conserved in mammals but n

171 terogeneous disease, resulting from cellular senescence, genetic predisposition and environmental fac

172 Delayed plant senescence had no effect, but a six-week delay in snow-o

173 ore, we highlight the evidence that cellular senescence has a causative role in multiple diseases ass

174 In recent years, cellular senescence has generated a lot of interest among researc

175 In particular, the occurrence of song senescence has rarely been demonstrated.

176 st 20 years, various identifiers of cellular senescence have been used to quantify the abundance of t

177 keletal muscle lamin A/C to prevent cellular senescence, IL-6 expression, hyperosteoclastogenesis, an

178 Finally, we focus on the role of cellular senescence in a number of endocrine diseases, including

179 find that neither the onset nor the rate of senescence in body mass or reproductive output shows cle

180 es when combined lead to similar patterns of senescence in both sexes.

181 that, contrary to human SCs, do not undergo senescence in culture.

182 stages revealed hypermethylation during leaf senescence in dml3 compared with WT, and 20 556 differen

183 effects on oxidative stress-induced cellular senescence in endothelial cells and skin fibroblasts.

184 intrasexual competition to increase rates of senescence in females-who are hormonally masculinized an

185 ransplantation, the donor mast cell-mediated senescence in FRCs was associated with collagen 1 deposi

186 use Hi-C to show that oncogenic RAS-induced senescence in human diploid fibroblasts is accompanied b

187 SC-EVs) on oxidative stress-induced cellular senescence in human endothelial cells and skin fibroblas

188 rmittent hypoxia (IH), a hallmark of OSA, on senescence in human white preadipocytes.

189 and associated oxidative stress might induce senescence in joint tissue cells.

190 current literature on the impact of cellular senescence in NAFLD/NASH and discuss the effectiveness a

191 Systemic induction of senescence in nontumor-bearing p16-3MR mice using a chem

192 implicates a transient state associated with senescence in normal epithelial tissue repair and its ab

193 en aged between 2 and 7 y experienced faster senescence in offspring survival in old age.

194 t phenocopies or rescues mTOR activation and senescence in PGAM5(-/-) cells, respectively.

195 d transcriptome changes during seasonal leaf senescence in Populus trichocarpa Nisqually-1, the Popul

196 man endothelial cells undergoing replicative senescence in presence of metformin.

197 ecular switch that determines the effects of senescence in prostate cancer.

198 reviously showed DNA damage, aneuploidy, and senescence in somatotroph adenomas, we studied links bet

199 Targeting senescence in the BMAd or other bone marrow cells may re

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

201 l studies have emphasized the involvement of senescence in the pathogenesis and development of liver

202 thritic effects associated with induction of senescence in the synovial tissue and cartilage protecti

203 ification of genes involved in seasonal leaf senescence in trees, and informs efforts to explore the

204 tential strategies to prevent and/or reverse senescence in tumor-specific T cells.

205 accelerated retinal pigment epithelial (RPE) senescence in vitro and in vivo.

206 eting genome replication to prevent cellular senescence in yeast, humans, and most other eukaryotes.

207 oductive senescence) and survival (actuarial senescence) in most organisms.

208 cargo SASP factors originating from multiple senescence inducers and cell types.

209 lung adenocarcinoma that are treated with a senescence-inducing combination of drugs, and restore ti

210 F, inflammation, and tissue damage caused by senescence-inducing irradiation and/or acetaminophen-ind

211 iew, we analyze the therapeutic relevance of senescence induction by CDK4/6 inhibitors.

212 e in senescence, the contribution of TRF1 to senescence induction has not been determined.

213 e select genetic and epigenetic elements for senescence induction have been identified, the dynamics,

214 e to taxol or DDM; 3) reduced propensity for senescence induction relative to DDM; 4) superior long-t

215 pe 2 diabetes impairs DNA repair, leading to senescence, inflammatory phenotypes, and ultimately fibr

216 en four major developmental phases - growth, senescence initiation, reorganization, and senescence te

217 Cellular senescence is a candidate mechanism that might be import

218 Cellular senescence is a contributor to intervertebral disc (IVD)

219 Cellular senescence is a primary aging process and tumor suppress

220 Senescence is a stress response that can be induced by s

221 Cellular senescence is a stress response that elicits a permanent

222 Senescence is characterized by a stable cell cycle arres

223 Leaf senescence is driven by the expression of senescence-ass

224 In addition, CPT-induced cellular senescence is facilitated by the expression of MIB1 and

225 vidence suggests that the complex process of senescence is involved in the development of a plethora

226 tent as a widespread concomitant of cellular senescence is reviewed.

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

228 Aging, or senescence, is a progressive deterioration of physiologi

229 study identifies chronic IH as a trigger of senescence-like phenotype in preadipocytes.

230 Rigosertib induced a senescence-like phenotype in the small percentage of sur

231 e develop a spontaneous pro-inflammatory and senescence-like phenotype.

232 ncer Cell, Kurppa et al. demonstrated that a senescence-like state enables lung cancer cells to survi

233 expression drives post-pregnancy MECs into a senescence-like state, and perturbations of this state i

234 velop impaired self-renewal with features of senescence, limiting complete repair.

235 stic studies reveal an elevation of cellular senescence marked by senescence-associated beta-galactos

236 ckout mice had no effect on the magnitude of senescence markers but associated with enhanced kidney d

237 ficantly improved inflammation, reduction in senescence markers in older mice, lipid peroxidation, an

238 In vivo, senescence markers were also increased in the bone marro

239 showed reduced p16INK4a protein and reduced senescence markers, confirming susceptibility to transfo

240 mere dysfunction, and adaptive immune system senescence may also contribute to frailty.

241 ge and discuss their interplay with cellular senescence, mitotic catastrophe, and autophagy.

242 ls, thus expanding our insight into the cell senescence molecular machinery.

243 y a permanent proliferation arrest, cellular senescence occurs in response to endogenous and exogenou

244 and metabolite analyses during dark-induced senescence of Arabidopsis (Arabidopsis thaliana) mutants

245 ine and l-methionine, to inhibit postharvest senescence of broccoli.

246 rance, cell growth retardation, and cellular senescence of DC fibroblasts.

247 treatment with quercetin alleviated cellular senescence of dermal fibroblasts.

248 CDKN1A, which has been known to promote senescence of fibroblasts but not melanocytes, is implic

249 n steatosis, concomitant with activation and senescence of hepatic stellate cells (HSCs), exhibiting

250 uction of OsSGR in indica, which accelerated senescence of indica rice cultivars.

251 re in iron protein maturation leads to early senescence of the bacteroids.

252 happen at different stages of the growth and senescence of the cell and during nuclear inversion even

253 We propose that senescence of the current allele is a cause of adaptive

254 In turn, cortisol production is affected by senescence of the hypothalamic-pituitary-adrenal (HPA) a

255 discusses which of the processes - cellular senescence or AD - might come first.

256 ensation, whereas others do so by subverting senescence or tumor-suppressor pathways.

257 in different cell fates such as quiescence, senescence, or apoptosis.

258 This factor appeared to play a key role in senescence-paracrine signaling.

259 role of reproductive competition in driving senescence, particularly when other differences between

260 However, senescence patterns can be highly variable across specie

261 rstand the substantial variation observed in senescence patterns in wild populations.

262 Annual reproductive success and senescence patterns vary substantially among individuals

263 ptor (MC(1)), synovial fibroblasts acquire a senescence phenotype characterized by arrested prolifera

264 s in the cytosol, which leads to a premature senescence phenotype.

265 ATG5 in HCT-116 cells increased 11G5-induced senescence, promoting proliferation of uninfected cells.

266 We also build cellular senescence protein-protein interaction and co-expression

267 y help explain among-individual variation in senescence rates in other species, including humans.

268 ameters also reveal novel potential cellular senescence regulators.

269 ity and used them to study subpopulations of senescence-related cells, demonstrating their dynamics,

270 data suggest that OSA may be considered as a senescence-related disorder.

271 gulates the expression of SAGs and thus leaf senescence remain elusive.

272 le in gene regulation but their relevance in senescence remains elusive.

273 These results suggest that RAS-induced senescence represents a cell fate determination-like pro

274 howed subsequent increased rate of actuarial senescence, resulting in reduced residual life span.

275 wering drug metformin exerts a valuable anti-senescence role.

276 PAD), membrane thermostability (MT), rate of senescence (RS), stay green trait (SGT), and NDVI values

277 Physiologically, senescence serves as a tumour-suppressive mechanism that

278 By contrast, analyses of actuarial senescence showed no cost of early-life reproduction.

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

280 ernal effects, we found that maternal effect senescence significantly reduces fitness for B. manjavac

281 larized epithelial cell type maintained at a senescence state, and offers an ideal cell model to stud

282 biological processes, including cell cycle, senescence, stress and interferon responses, epithelial-

283 Rather, it increases hallmarks of senescence such as senescence-associated beta-galactosid

284 , senescence initiation, reorganization, and senescence termination.

285 ify several candidate biomarkers of cellular senescence that overlap with aging markers in human plas

286 sstalk between hepatocyte metabolism and HSC senescence that promotes tumour growth.

287 es contributes to the DNA damage response in senescence, the contribution of TRF1 to senescence induc

288 VHD pathogenesis and stress-induced cellular senescence through the senescence-associated secretory p

289 lling was correlated with flowering time and senescence to create a range of seasonal life-history sy

290 TIMP1 deletion allows senescence to promote metastasis, and elimination of sen

291 wild populations have compared sex-specific senescence trajectories outside of polygynous species, m

292 undergoing replicative or palmitate-induced senescence versus healthy aortic VSMCs.

293 Biliary senescence was determined by immunofluorescence and sene

294 In addition, increased senescence was observed in the kidneys of animals admini

295 ter understand the molecular control of leaf senescence, we examined transcriptome changes during sea

296 dence of telomerase activation in HBECs near senescence when telomeres are critically short.

297 ondrial dynamics has been linked to cellular senescence, which contributes to advanced age-related di

298 didates tested induce at least one marker of senescence with 13 genes (C9orf40, CDC25A, CDCA4, CKAP2,

299 tivars in Korean rice fields lead to delayed senescence, with increased grain yield and enhanced phot

300 le properties such as mass, maintenance, and senescence, yet leaving reaction-level behavior unconstr