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Mechanisms of cellular senescence in human and mouse cells.
Abstract
Telomere erosion is considered to be the main cause of the onset of replicative senescence. However, recent findings suggest that a senescent phenotype can be induced by a variety of other stimuli that act independently of telomeres. Moreover, telomere-dependent replicative senescence depends on the species of cell origin, in particular whether cells are of human or rodent origin. In addition, the tissue of origin may also dictate the pathway by which cells undergo replicative senescence. In this Review article, we categorize cellular senescence into two types, which for simplicity we term intrinsic or extrinsic senescence, focus on the differences between human and mouse cells, and discuss the roles of the p53 and pRb tumor suppressor pathways in cellular senescence.
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“Previous studies illustrated that in vitro cultivated senescent MEFs manifested upregulation of Cdkn1a (encoding p21), Cdkn2a (encoding p16), Lmnb1, Mki67, and other conventional senescence markers (Sherr and Dipinho, 2000; Parrinello et al., 2003; Itahana et al., 2004).”
From Single-Cell Transcriptome Analysis Reveals Six Subpopulations Reflecting Distinct Cellular Fates in Senescent Mouse Embryonic Fibroblasts (2020) · cites this paper as Itahana et al., 2004
In the citing paper
“MEFs derived from M. musculus possess long telomeres and easily detectable telomerase activity (Itahana et al., 2004”
From DNA Repair, Genome Stability, and Aging (2005) · cites this paper as Itahana et al., 2004
In the citing paper
“In many primary human cell lines, replicative senescence occurs secondary to attrition of the ends of the chromosomes, the telomeres, in a process termed “intrinsic senescence” (Itahana et al., 2004”
From DNA Repair, Genome Stability, and Aging (2005) · cites this paper as Itahana et al., 2004
In the citing paper
“senescent cells accumulate in vivo in mammals with increasing age and at sites of pathology (Itahana et al., 2004”
From DNA Repair, Genome Stability, and Aging (2005) · cites this paper as Itahana et al., 2004
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“Extensive telomere shortening activates the p53 and retinoblastoma protein pathways, resulting in cellular proliferation arrest and senescence (Itahana et al., 2004).”
BackgroundTelomeres and telomerase in adrenocortical tissue maintenance, carcinogenesis, and aging
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“…as after eight to ten population doublings, and the progression to senescence is believed to be mainly driven by the accumulation of ongoing DNA damage as it can be prevented by low oxygen culture conditions (Kipling & Cooke 1990, Prowse & Greider 1995, Parrinello et al. 2003, Itahana et al. 2004).”
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Sahabi, S., Jafari-Gharabaghlou, D., & Zarghami, N. (2022) · Acta Histochemica · doi:10.1016/j.acthis.2021.151841 · Cited by 16
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“In contrast, extrinsic telomere-independent senescence results from diverse stimuli, including ultraviolet radiation, oxidative stress, oncogene activation, and proinflammatory cytokines (10-12).”
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“com 583 AGING SA-β-gal assay has been viewed as the gold standard for identification of senescent cells [44–46] and has been the most extensively utilized biomarker for senescent cells in vitro and in vivo [47, 48].”
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BackgroundLong-Term Culture of Human Gingival Keratinocyte Progenitor Cells by Down-regulation of 14-3-3 σ
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Kiyokawa, H. (2006) · Springer eBooks · doi:10.1007/400_001 · Cited by 10
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“Other commonly used markers include cyclin‐ dependent kinase inhibitors p16 and p21, both which induce cell cycle arrest by hindering DNA replication.(43,44) In our study, significant increases in the percentage of β‐gal positive cells and expression levels of p16 and p21 occurred in both HH40 and HH42 cells at higher…”
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Backgroundde Aquino, L. V. C., Olindo, S. L., Silva, Y. L. F. E., de Oliveira, L. R. M., Moura, Y. B. F., Rodrigues, A. L. R., Praxedes, É. A., de Oliveira, M. F., Silva, A. R., & Pereira, A. F. (2024) · Acta Histochemica · doi:10.1016/j.acthis.2024.152185 · Cited by 4
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BackgroundTrubitsyn, A. G. (2013) · Advances in Gerontology · doi:10.1134/s2079057013030120 · Cited by 4
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Meang, M. K., Kim, S., Kim, I. H., Kim, H.-S., & Youn, B. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23126852 · Cited by 3
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“As a result, after a certain number of doublings, the telomere end is depleted and divisions are terminated due to chromosome erosion [ 17 ].”
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Gallic acid ameliorates thymic involution via activating Sox2 and Nanog
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“Given the differences between human and mouse senescence (Itahana et al., 2004; Kennedy et al., 2010), it would be significant if SADS constitutes a hallmark common to both species.”
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Background
Metadata
- Authors
- Itahana, K., Campisi, J., & Dimri, G. P.
- Affiliations
- The University of Texas MD Anderson Cancer Center (US)
- Lawrence Berkeley National Laboratory (US)
- Corresponding author
- Dimri, Goberdhan P.
- Venue
- Biogerontology
- Published
- 2004-02
- Volume
- 5
- Issue
- 1
- Pages
- 1-10
- ISSN
- 1389-5729 (ISSN-L)
- 1573-6768
- OpenAlex
- W2036676765
- Cited by
- 338
- References
- 83
- Citations by year
- 2026: 5 · 2025: 7 · 2024: 4 · 2023: 9 · 2022: 19 · 2021: 11 · 2020: 13 · 2019: 14 · 2018: 14 · 2017: 10 · 2016: 16 · 2015: 14 · 2014: 13 · 2013: 23 · 2012: 19
- FWCI
- 2.63
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- Biogerontology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- cellular senescence, replicative senescence, telomere shortening, p53 pathway, pRb pathway, tumor suppressor pathways, tissue of origin, senescence mechanisms
- MeSH terms
- Animals, Humans, Nuclear Proteins, Proto-Oncogene Proteins, Repressor Proteins, Tumor Suppressor Protein p53, Retinoblastoma Protein, Telomere, Cellular Senescence, Cyclin-Dependent Kinase Inhibitor p16, Mice, Polycomb Repressive Complex 1
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