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  1. 4141
    “…PRMT5 knockdown significantly triggered pronounced senescence in OS cells, as evidenced by the increase in senescence-associated β-galactosidase (SA-β-gal)-stained cells, induction of p21 expression, and upregulation of senescence-associated secretory phenotype (SASP) gene expression. …”
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  2. 4142
    “…Our data revealed that insulin impeded osteogenesis of BMSCs by inhibiting autophagy and promoting premature senescence, which it should be responsible for T2DM-induced bone loss, at least in part. …”
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  3. 4143
    “…The accumulation of senescent cells (SnCs) is a causal factor of various age‐related diseases as well as some of the side effects of chemotherapy. …”
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  4. 4144
    “…We test the prediction that—contrary to the faster or earlier senescence under predation risk that increases with prey size and age—under predation risk that decreases with prey size and age either no senescence acceleration or even its deceleration is to be observed. …”
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  5. 4145
    “…In contrast, the expression of two marker genes involved in the nodule senescence, Cysteine Protease 6 and Purple Acid Protease, increased significantly in mutant nodules at 10 dpi strengthening the idea that an early senescence process occurs in SmgshB nodules. …”
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  6. 4146
    “…To ensure genomic integrity, the irreparable cells in a population exit permanently from the cell cycle, and this process is termed “senescence.” However, senescence only blocks the expansion of unwanted cells, and the aberrant chromatin of senescent cells remains unstable. …”
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  7. 4147
    “…The aim of this study was to determine the role of proteasomal system and heat shock proteins to maintain proteome balance during replicative senescence in mild hyperthermia conditions. Our results demonstrated that HSP40/70 machinery is induced by mild hyperthermia conditions independent from senescence conditions. …”
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  8. 4148
  9. 4149
    “…SENEBLOC was shown to block the induction of cellular senescence through dual mechanisms that converge to repress the expression of p21. …”
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  10. 4150
    “…BACKGROUND: Recent studies have suggested that hepatocyte senescence could contribute to hepatic steatosis and its progression in nonalcoholic fatty liver disease (NAFLD). …”
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  11. 4151
    “…BACKGROUND: Freshly isolated mouse embryonic fibroblasts (MEFs) have great proliferation capacity but quickly enter senescent state after several rounds of cell cycle, a process called premature senescence. …”
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  12. 4152
    “…The treatment with PMD induced erythrocytes senescence which can be hypothesized to account for the physiological effect of disseminated PLPs in loss of circulating erythrocytes inducing malaria anemia. …”
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  13. 4153
    “…Prelamin A, an abnormal processed form of the nuclear lamina protein lamin A, has been reported to trigger premature senescence. However, the mechanism driving stem cell dysfunction is still unclear. …”
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  14. 4154
    “…These changes and the reversible nature of the senescence state were consistent with epigenetic regulation; thus, it was investigated as to whether the senescent state could be reversed by epigenetic inhibitors. …”
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  15. 4155
  16. 4156
    “…BACKGROUND: The primary purpose of this study was to investigate the protective effect of metformin against hydrogen peroxide (H(2)O(2))-induced cellular senescence and to explore the underlying molecular mechanism of lens epithelial cell senescence. …”
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  17. 4157
    “…The current research aimed to explore the possible relationship between PINK1/PARKIN‐mediated mitophagy and the compression‐induced senescence of nucleus pulposus cells (NPCs). Therefore, the stages of senescence in NPCs were measured under compression lasting 0, 24 and 48 hours. …”
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  18. 4158
    “…Long-term stimulation with selected microalgal extracts attenuated the development of oxidative stress-induced senescence in skin cells that, at least in part, was correlated with nitric oxide signaling and increased niacin and biotin levels compared to an unmodified microalgal clone. …”
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  19. 4159
    “…ESC‐sEVs treatment ameliorates H‐NSCs senescence by inhibiting mTORC1 activation, and promoting TFEB nuclear translocation and lysosome resumption, thereby reversing senescence‐related neurogenesis dysfunction and cognitive impairment in VD. …”
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  20. 4160
    “…Accumulation of progerin causes nuclear abnormalities and cell cycle arrest ultimately leading to cellular senescence. Autophagy impairment is a hallmark of cellular aging, and the rescue of this proteostasis mechanism delays aging progression in HGPS cells. …”
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