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  1. 1981
    “…Mature human erythrocytes circulate in blood for approximately 120 days, and senescent erythrocytes are removed by splenic macrophages. …”
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  2. 1982
  3. 1983
    “…However, no systematic identification of circRNAs associated with leaf senescence in rice has been studied. In this study, a genome-wide high-throughput sequencing analysis was performed using rice flag leaves developing from normal to senescence. …”
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  4. 1984
    “…Accumulation of senescent cells accompanied by an impairment in the immune-mediated elimination mechanisms results in increased frequency of senescent cells, termed “chronic” senescence. …”
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  5. 1985
    “…This study purposed to evaluate the change of telomere length and senescence markers during human ovarian tissue cryopreservation. …”
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  6. 1986
  7. 1987
    “…Cellular repressor of E1A-stimulated genes 1 (CREG1) is a secreted glycoprotein that accelerates p16-dependent cellular senescence in vitro. We recently reported the ability of CREG1 to stimulate brown adipogenesis using adipocyte P2-CREG1-transgenic (Tg) mice; however, little is known about the effect of CREG1 on aging-associated phenotypes. …”
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  8. 1988
    “…In this manuscript, we review current knowledge regarding a cellular state that increases the risk of genomic destabilization, in which cells exhibit phenotypes often observed during senescence. In addition, we explore the pathways that lead to genomic destabilization and its associated mutagenesis, which ultimately result in cancer.…”
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  9. 1989
    “…Cellular senescence is a complex stress response that induces an essentially permanent cell cycle arrest and a complex secretory phenotype termed the senescence‐associated secretory phenotype (SASP), which drives numerous aging pathologies. …”
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  10. 1990
    “…Vascular smooth muscle cell (VSMC) senescence promotes atherosclerosis and features of plaque instability, in part, through lipid-mediated oxidative DNA damage and telomere dysfunction. …”
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  11. 1991
    “…Furthermore, tumor-derived ILT4/PIR-B (ILT4 ortholog in mouse) is directly involved in induction of cell senescence in naïve/effector T cells mediated by tumor cells in vitro and in vivo. …”
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  12. 1992
    “…Human lung fibroblasts (HLFs) were treated with CoCl(2) or hypoxia to induce cellular senescence in vitro. SA-β-gal staining and the changes of senescent markers were used to examine cellular senescence. …”
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  13. 1993
    “…We also found that captopril decreased markers for radiation-induced accelerated senescence in the lung tissue. Our data suggest that suppression of inflammation and senescence markers, combined with an increase of anti-inflammatory factors, are a part of the mechanism for captopril-induced survival in thoracic irradiated mice.…”
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  14. 1994
    “…Although senescent cells display various morphological changes including vacuole formation, it is still unclear how these processes are regulated. …”
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  15. 1995
    “…Accumulation of senescent cells in tissues during normal or accelerated aging has been shown to be detrimental and to favor the outcomes of age-related diseases such as heart failure (HF). …”
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  16. 1996
  17. 1997
    “…FINDINGS: The expressions of cellular senescence marker were observed in the sarcomatous component of the patient with long-term survival but not observed in the other patients with short- term survival. …”
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  18. 1998
    “…The observed increase in the levels of senescence markers suggested that FZD5 knockdown promotes cellular senescence by regulating the noncanonical Wnt pathway. …”
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  19. 1999
    “…The two dominant mechanisms of senescence include replicative senescence, predominantly depending on age-induced telomere shortening, and stress-induced senescence, triggered by external or intracellular harmful stimuli. …”
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  20. 2000
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