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  1. 4841
    por Oh, D, Park, S, Jo, C, Yoo, H
    Publicado 2012
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    P01.13. Assessing cognitive decline and cardiac senescence in middle aged and elderly volunteers: implications for herbal medicine utilization
  2. 4842
    “…Overexpression of CTGF induces HIF-1α-dependent metabolic alterations, with the induction of autophagy/mitophagy, senescence, and glycolysis. Here, we show that CTGF exerts compartment-specific effects on tumorigenesis, depending on the cell-type. …”
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    CTGF drives autophagy, glycolysis and senescence in cancer-associated fibroblasts via HIF1 activation, metabolically promoting tumor growth
  3. 4843
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    Rutin, a Flavonoid That Is a Main Component of Saussurea involucrata, Attenuates the Senescence Effect in D-Galactose Aging Mouse Model
  4. 4844
    “…Our findings serve as indications of cellular senescence on a molecular level, while it seems that these cells are less easily stimulated in vitro in order to duplicate.…”
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    Transcription of the Tumor Suppressor Genes p53 and RB in Lymphocytes from Patients with Chronic Kidney Disease: Evidence of Molecular Senescence?
  5. 4845
    “…Taken together, our current findings suggest that the miR-29 upregulated in aging may be involved in the downregulation of type IV collagen, leading to a possible weakening of the basal membrane in senescent tissues, and miR-29 may be a useful molecular marker of senescence.…”
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    Reduction of Type IV Collagen by Upregulated miR-29 in Normal Elderly Mouse and klotho-Deficient, Senescence-Model Mouse
  6. 4846
    “…BACKGROUND: Cellular senescence represents a tumor suppressive response to a variety of aberrant and oncogenic insults. …”
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    Temporally distinct roles for tumor suppressor pathways in cell cycle arrest and cellular senescence in Cyclin D1-driven tumor
  7. 4847
    “…Serial passage-induced senescence in RVSMCs and HACs was able to be significantly prevented at 50 μM EGCG, while in HDFs, 100 μM EGCG could significantly prevent senescence and recover their cell cycle progression close to the normal level. …”
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    Preventive Effects of Epigallocatechin-3-O-Gallate against Replicative Senescence Associated with p53 Acetylation in Human Dermal Fibroblasts
  8. 4848
    “…Apoptosis, autophagy, necrosis and cellular senescence are key responses of cells that were exposed to genotoxicants. …”
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    Survival and Death Strategies in Glioma Cells: Autophagy, Senescence and Apoptosis Triggered by a Single Type of Temozolomide-Induced DNA Damage
  9. 4849
    “…Previously, we identified partial env sequences of new xenotropic MuLVs (X-MuLVs) from a senescence-accelerated mouse (SAM) strain. In the present study, we investigated and characterized the complete sequences of the X-MuLVs. …”
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    Complete Genome Sequences of New Xenotropic Murine Leukemia Viruses from the Senescence-Accelerated Mouse (SAM): Molecular and Phylogenetic Analyses
  10. 4850
    por Liu, Fang, Guo, Fang-Qing
    Publicado 2013
    “…Nitric oxide (NO) has been known to preserve the level of chlorophyll (Chl) during leaf senescence. However, the mechanism by which NO regulates Chl breakdown remains unknown. …”
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    Nitric Oxide Deficiency Accelerates Chlorophyll Breakdown and Stability Loss of Thylakoid Membranes during Dark-Induced Leaf Senescence in Arabidopsis
  11. 4851
    “…Expression of the alternatively spliced ING1a tumor suppressor increases >10-fold during replicative senescence. ING1a overexpression inhibits growth; induces a large flattened cell morphology and the expression of senescence-associated β-galactosidase; increases Rb, p16, and cyclin D1 levels; and results in the accumulation of senescence-associated heterochromatic foci. …”
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    The ING1a Tumor Suppressor Regulates Endocytosis to Induce Cellular Senescence Via the Rb-E2F Pathway
  12. 4852
    “…The underlying cause of senescence due to replicative exhaustion is telomere shortening. …”
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    How to measure RNA expression in rare senescent cells expressing any specific protein such as p16(Ink4a)
  13. 4853
    “…At a long term, a reduction in clonogenic capacity was observed, accompanied by a large induction of senescence. CONCLUSION: The presence of Rsv forces cells treated with TMZ through mitosis leading to mitotic catastrophe and senescence, reducing the clonogenic capacity of glioma cells and increasing the chronic effects of temozolomide.…”
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    Resveratrol abrogates the Temozolomide-induced G2 arrest leading to mitotic catastrophe and reinforces the Temozolomide-induced senescence in glioma cells
  14. 4854
    por Jia, Yanxia, Tao, Faqing, Li, Weiqi
    Publicado 2013
    “…Senescence is the last phase of the plant life cycle and has an important role in plant development. …”
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    Lipid Profiling Demonstrates That Suppressing Arabidopsis Phospholipase Dδ Retards ABA-Promoted Leaf Senescence by Attenuating Lipid Degradation
  15. 4855
    “…Reactive oxygen species (ROS) can induce premature cellular senescence, which is believed to contribute to aging and age-related diseases. …”
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    Inhibition of nuclear factor-erythroid 2–related factor (Nrf2) by caveolin-1 promotes stress-induced premature senescence
  16. 4856
    “…Additionally a subset of primary and cancer cells was accelerated into senescence by oxidative stress. DNA methylation and chromatin condensation levels decreased with declining doubling times when primary cells aged in culture with the lowest levels reached at the stage of proliferative senescence. …”
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    Nuclear DNA Methylation and Chromatin Condensation Phenotypes Are Distinct Between Normally Proliferating/Aging, Rapidly Growing/Immortal, and Senescent Cells
  17. 4857
    por Strozyk, Elwira, Kulms, Dagmar
    Publicado 2013
    “…Alternatively, p53 irreversibly blocks cell cycle progression to prevent AKT/mTOR-driven proliferation, thereby inducing premature senescence. Conclusively, AKT/mTOR via an extensive cross talk with p53 influences the UV response in the skin with no black and white scenario deciding over death or survival.…”
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    The Role of AKT/mTOR Pathway in Stress Response to UV-Irradiation: Implication in Skin Carcinogenesis by Regulation of Apoptosis, Autophagy and Senescence
  18. 4858
    “…In previous studies increased hepatocyte nuclear area and hepatocyte expression of p21, both markers of senescence, were associated with increased fibrosis stage and a poor outcome in non-alcohol-related fatty liver disease, while increased hepatocyte nuclear area was related to liver dysfunction in ALD cirrhosis. …”
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    Hepatocyte Expression of the Senescence Marker p21 Is Linked to Fibrosis and an Adverse Liver-Related Outcome in Alcohol-Related Liver Disease
  19. 4859
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    Therapeutic and space radiation exposure of mouse brain causes impaired DNA repair response and premature senescence by chronic oxidant production
  20. 4860
    “…TGF-β1 did not induce premature senescence. However, due to increased proliferation rates the cells reached replicative senescence earlier than untreated controls. …”
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    TGF-beta1 Does Not Induce Senescence of Multipotent Mesenchymal Stromal Cells and Has Similar Effects in Early and Late Passages
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