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  1. 1881
    “…In addition to promoting various forms of cell death, most conventional anti-tumor therapies also promote senescence. There is now extensive evidence that therapy-induced senescence (TIS) might be transient, raising the concern that TIS could represent an undesirable outcome of therapy by providing a mechanism for tumor dormancy and eventual disease recurrence. …”
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    Non-Cell Autonomous Effects of the Senescence-Associated Secretory Phenotype in Cancer Therapy
  2. 1882
    “…AIM: In the present study, attempts have been made to explore the differential response of young and senescent erythrocytes separated by density gradient centrifugation from accelerated senescence model of rats mimicking Hutchinson-Gilford progeria syndrome and naturally aged rats. …”
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    Erythrocyte Senescence in a Model of Rat Displaying Hutchinson-Gilford Progeria Syndrome
  3. 1883
    “…Cigarette smoke (CS) induces lung cellular senescence that plays an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD). …”
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    Lung cellular senescence is independent of aging in a mouse model of COPD/emphysema
  4. 1884
    por Robinson, Andria R., Yousefzadeh, Matthew J., Rozgaja, Tania A., Wang, Jin, Li, Xuesen, Tilstra, Jeremy S., Feldman, Chelsea H., Gregg, Siobhán Q., Johnson, Caroline H., Skoda, Erin M., Frantz, Marie-Céline, Bell-Temin, Harris, Pope-Varsalona, Hannah, Gurkar, Aditi U., Nasto, Luigi A., Robinson, Renã A.S., Fuhrmann-Stroissnigg, Heike, Czerwinska, Jolanta, McGowan, Sara J., Cantu-Medellin, Nadiezhda, Harris, Jamie B., Maniar, Salony, Ross, Mark A., Trussoni, Christy E., LaRusso, Nicholas F., Cifuentes-Pagano, Eugenia, Pagano, Patrick J., Tudek, Barbara, Vo, Nam V., Rigatti, Lora H., Opresko, Patricia L., Stolz, Donna B., Watkins, Simon C., Burd, Christin E., Croix, Claudette M. St., Siuzdak, Gary, Yates, Nathan A., Robbins, Paul D., Wang, Yinsheng, Wipf, Peter, Kelley, Eric E., Niedernhofer, Laura J.
    Publicado 2018
    “…Accumulation of senescent cells over time contributes to aging and age-related diseases. …”
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    Spontaneous DNA damage to the nuclear genome promotes senescence, redox imbalance and aging
  5. 1885
    “…We conclude that senescence-associated miRNAs are involved in the decline of NRF2 expression, thus contributing to the repression of adaptive responses during cell senescence.…”
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    MicroRNAs mediate the senescence-associated decline of NRF2 in endothelial cells
  6. 1886
    “…Critical Issues: The culture expansion needed before MSC transplantation is associated with cellular senescence. Moreover, accelerated senescence of the total and perivascular MSC pool has been observed in humans and mouse models of premature aging disorders. …”
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    Oxidative Stress in Mesenchymal Stem Cell Senescence: Regulation by Coding and Noncoding RNAs
  7. 1887
    “…In old age, however, the senescence rate was stronger in males that showed high demographic performance at younger ages. …”
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    From early life to senescence: individual heterogeneity in a long‐lived seabird
  8. 1888
    “…These senescent cells acquired the senescence-associated secretory phenotype (SASP). …”
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    Chromosomal instability-induced senescence potentiates cell non-autonomous tumourigenic effects
  9. 1889
    “…However, the link between the senescence-like phenotype and the resistance to BRAF inhibition is not fully understood yet. …”
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    Acquired resistance to BRAFi reverses senescence-like phenotype in mutant BRAF melanoma
  10. 1890
    “…Both nitric oxide (NO) and calcium ion (Ca(2+))/calmodulin (CaM) have been shown to regulate the senescence of cut flowers. However, not much is known about the crosstalk between NO and Ca(2+)/CaM during the senescence of cut flowers. …”
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    Involvement of Calcium and Calmodulin in Nitric Oxide-Regulated Senescence of Cut Lily Flowers
  11. 1891
    “…CONCLUSIONS: Inflammation-induced Gro1 triggers neuroblast senescence, thus suppressing new neuron development in the hippocampus. …”
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    Inflammation-induced Gro1 triggers senescence in neuronal progenitors: effects of estradiol
  12. 1892
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    Clearance of senescent glial cells prevents tau-dependent pathology and cognitive decline
  13. 1893
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    Early Senescence and Leukocyte Telomere Shortening in SCHIZOPHRENIA: A Role for Cytomegalovirus Infection?
  14. 1894
    “…The paramount role of senescent cells in ageing has prompted suggestions that re-expression of telomerase may prevent ageing; a proposition that is predicated on the assumption that senescent cells are the sole cause of ageing. …”
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    Epigenetic ageing is distinct from senescence-mediated ageing and is not prevented by telomerase expression
  15. 1895
    “…Among these senescence-up-regulated NtNACs, NtNAC080, a close homolog of AtNAP, is a positive regulator of leaf senescence. …”
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    NAC Family Transcription Factors in Tobacco and Their Potential Role in Regulating Leaf Senescence
  16. 1896
    “…By means of the mutations of the telomerase reverse transcriptase (TERT) promoter and ATRX/DAXX, cancers can immortalize and escape cell senescence and apoptosis. In this article, we review the evidence for triggering GBM cell death by targeting telomerase and the ALT pathway, with an extra focus on a plant-derived compound, butylidene phthalide (BP), which may be a promising novel anticancer compound with good potential for clinical applications.…”
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    Targeting Telomerase and ATRX/DAXX Inducing Tumor Senescence and Apoptosis in the Malignant Glioma
  17. 1897
    “…It has also become evident that senescence is a highly dynamic and heterogenous process. …”
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    Short-term gain, long-term pain: the senescence life cycle and cancer
  18. 1898
    “…In eukaryotes, telomeres determine cell proliferation potential by triggering replicative senescence in the absence of telomerase. In Saccharomyces cerevisiae, senescence is mainly dictated by the first telomere that reaches a critically short length, activating a DNA-damage-like response. …”
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    A subtelomeric region affects telomerase-negative replicative senescence in Saccharomyces cerevisiae
  19. 1899
    “…Senescence is a tumor-suppressive mechanism induced by telomere shortening, oncogenes, or chemotherapy treatment. …”
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    Regulation of senescence escape by TSP1 and CD47 following chemotherapy treatment
  20. 1900
    “…Primary myoblast culture from these patients demonstrated common findings consistent with reduced proliferation and differentiation, diminished satellite cell pool, accelerated senescence of muscle, and signs of autophagy activation.…”
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    Altered myogenesis and premature senescence underlie human TRIM32-related myopathy
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