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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“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
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“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…”
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“In mouse embryo fibroblasts and most human fibroblasts the p53 pathway is predominant; however, many human cells also invoke the Rb pathway via p16 ( Itahana et al., 2004 ).”
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Yeon, S. J. (2015) · eScholarship (California Digital Library)
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Pediatria, D. D., Dello, M., & Immunologia, I. E. E. (2008)
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Young, L. V., Cameron, A., Springer, S. S., Ross, J. P., Wolters, G., Murphy, J. P., Arsenault, M. G., Ng, S. Y., Ljubicic, V., & Johnston, A. P. W. (2020) · SSRN Electronic Journal · doi:10.2139/ssrn.3748740
Charley, J. (1988)
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“Other drivers of senescence are generally included in the second class termed “stress-induced premature senescence” (see Figures 1, 2, and 3) [18,20].”
BackgroundCharest, A., Wilker, E., McLaughlin, M. E., Lane, K. M., Gowda, R., Coven, S., McMahon, K., Kovach, S., Feng, Y., Yaffe, M. B., et al. (2023) · doi:10.1158/0008-5472.c.6494688
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“As compared to human cells, fewer genetic lesions are required to transform mouse cells (Hahn 2002; Itahana et al. 2004).”
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Markina, Y. V., Kirichenko, T. V., Zhivodernikov, I. V., Markin, A. M., Eremin, I. I., Deev, R. V., & Kotenko, K. V. (2025) · I P Pavlov Russian Medical Biological Herald · doi:10.17816/pavlovj634546
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“240 The fi rst clinical trials using senolytics for conditions such as Alzheimer ’ s disease or idiopathic pulmonary fi brosis suggest that these drugs are safe and tolerable, but the functional impact remains to be determined.”
Melatonin as a radioprotectant against mitochondrial damage
Shimura, T., Wu, J., Aizawa, M., Takahashi, Y., Sasatani, M., Nakamura, A., & Ushiyama, A. (2026) · International Journal of Radiation Biology · doi:10.1080/09553002.2026.2636299
“Radiation can also kill fibroblasts by accelerating senescence (Itahana et al. 2004).”
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“Circulating and tissue-based markers index senescent-cell burden and SASP intensity (SA-β -galactosidase, lipofuscin, senescence-associated heterochromatic foci, circulating IL-6/GDF-15/PAI-1, p16INK4a-positive cells) [12, 33, 34].”
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Self-citationLysosomal Involvement in the Pathogenesis of Alzheimer's Disease
Zheng, L. P. (2012) · DiVA (Linkoping University)
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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