The DOI matches its Crossref record; 82 of the 83 references it cites were found in a registry or an index.
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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In the citing paper
“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
Citations
Cites
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Self-citationTelomeres shorten during ageing of human fibroblasts
Harley, C. B., Futcher, A. B., & Greider, C. W. (1990) · Nature · doi:10.1038/345458a0 · Cited by 5,750
Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a
Serrano, M., Lin, A. W., McCurrach, M. E., Beach, D., & Lowe, S. W. (1997) · Cell · doi:10.1016/s0092-8674(00)81902-9 · Cited by 5,218 · cited 2×
“Moreover, p53 activity is enhanced by a variety of stresses such as DNA damage (Di Leonardo et al. 1994), oncogenic insults (Serrano et al. 1997), and quiescence by growth factor deprivation (Itahana et al. 2001; Itahana et al. 2002). p53 activation in response to stressful conditions causes cell…”
BackgroundExtension of Life-Span by Introduction of Telomerase into Normal Human Cells
Bodnar, A. G., Ouellette, M., Frolkis, M., Holt, S. E., Chiu, C.-P., Morin, G. B., Harley, C. B., Shay, J. W., Lichtsteiner, S., & Wright, W. E. (1998) · Science · doi:10.1126/science.279.5349.349 · Cited by 4,975
Pleiotropy, natural selection, and the evolution of senescence.
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Mammalian Telomeres End in a Large Duplex Loop
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Telomere Shortening and Tumor Formation by Mouse Cells Lacking Telomerase RNA
Blasco, M. A., Lee, H.-W., Hande, M. P., Samper, E., Lansdorp, P. M., DePinho, R. A., & Greider, C. W. (1997) · Cell · doi:10.1016/s0092-8674(01)80006-4 · Cited by 2,108
Pleiotropy, natural selection, and the evolution of senescence
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Research works printed but not linked: 2
- Campisi J, Dimri GP and Hara E (1996) Control of replicative senescence. In: Schneider EL and Rowe JW (eds) Handbook of the Biology of Aging, 4th ed, pp 121-149. Academic Press, San Diego, California
- Wright WE and Shay JW (1996) Mechanism of escaping senescence in human diploid cells. In: Holbrook NJ, Martin GR and Lockshin R (eds) Modern Cell Biology Series - Cellular Aging and Cell Death, pp 153-167. Wiley & Sons, New York
Cited by
Sorted by citations
Cellular senescence: when bad things happen to good cells
Campisi, J., & d'Adda di Fagagna, F. (2007) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2233 · Cited by 4,441
Self-citationBiochemistry of oxidative stress
Halliwell, B. B. (2007) · Biochemical Society Transactions · doi:10.1042/bst0351147 · Cited by 1,591
Oxidative stress and cancer: Have we moved forward?
Halliwell, B. (2007) · Biochemical Journal · doi:10.1042/bj20061131 · Cited by 1,302
DNA Repair, Genome Stability, and Aging
Lombard, D. B., Chua, K. F., Mostoslavsky, R., Franco, S., Gostissa, M., & Alt, F. W. (2005) · Cell · doi:10.1016/j.cell.2005.01.028 · Cited by 944
Exploiting senescence for the treatment of cancer
Wang, L., Lankhorst, L., & Bernards, R. (2022) · Nature Reviews Cancer · doi:10.1038/s41568-022-00450-9 · Cited by 867
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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