The DOI matches its Crossref record; 100 of the 102 references it cites were found in a registry or an index.
Impact of cellular senescence signature on ageing research
Abstract
Cellular senescence as the state of permanent inhibition of cell proliferation is a tumour-suppressive mechanism. However, due to the associated secretory phenotype senescence can also contribute to cancer and possibly other age-related diseases, such as obesity, diabetes, atherosclerosis and Alzheimer's disease. There are two major mechanisms of cellular senescence; replicative senescence depends on telomere erosion or dysfunction whilst stress-induced premature senescence (SIPS) is telomere-independent and also includes oncogene-induced senescence (OIS). The senescence phenotype is characterised by altered cellular morphology, increased activity for senescence-associated-β-galactosidase (SA-β-GAL), increased formation of senescence-associated heterochromatin foci (SAHF) and promyelocytic leukemia protein nuclear bodies (PML NBs), permanent DNA damage, chromosomal instability and an inflammatory secretome. Some of these markers have been identified in cells from age-related pathologies. However, to improve our understanding of the contribution of cellular senescence to organismal ageing and age-related disease, it is imperative to define an unequivocal signature of cellular senescence that is functionally connected with normal and pathological ageing. Herein, we describe the processes leading to senescence, and the current biomarkers of cellular senescence, with particular emphasis on the causal role of DNA damage responses involved in the process. We highlight the gaps in o…
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“Both normal and tumor cells undergo senescence in response to various insults that cause persistent DNA damage (Kuilman et al., 2010; Rodier and Campisi, 2011; Sikora et al., 2011; Ohtani and Hara, 2013)”
From Targeting Janus Kinases and Signal Transducer and Activator of Transcription 3 To Treat Inflammation, Fibrosis, and Cancer: Rationale, Progress, and Caution (2020) · cites this paper as Sikora et al., 2011
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Salminen, A., Kauppinen, A., & Kaarniranta, K. (2012) · Cellular Signalling · doi:10.1016/j.cellsig.2011.12.006 · Cited by 763
Sharma, R. K., Agarwal, A. K., Rohra, V. K., Assidi, M., Abu-Elmagd, M. M., & Turki, R. F. (2015) · Reproductive Biology and Endocrinology · doi:10.1186/s12958-015-0028-x · Cited by 486
Georgakopoulou, E., Tsimaratou, K., Evangelou, K., Fernandez, M.-P., Zoumpourlis, V, Trougakos, I., Kletsas, D., Bartek, J., Serrano, M., & Gorgoulis, V. (2012) · Aging · doi:10.18632/aging.100527 · Cited by 390
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Frasca, D., & Blomberg, B. B. (2016) · Biogerontology · doi:10.1007/s10522-015-9578-8 · Cited by 357
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Metadata
- Authors
- Sikora, E., Arendt, T., Bennett, M., & Narita, M.
- Affiliations
- Instytut Biologii Doświadczalnej im. Marcelego Nenckiego (PL)
- Leipzig University (DE)
- University of Cambridge (GB)
- Cancer Research UK (GB)
- Corresponding author
- Sikora, Ewa
- Venue
- Ageing Research Reviews
- Publisher
- Elsevier BV
- Published
- 2011-01
- Volume
- 10
- Issue
- 1
- Pages
- 146-152
- ISSN
- 1568-1637 (ISSN-L)
- OpenAlex
- W1977970646
- Cited by
- 264
- References
- 102
- Citations by year
- 2026: 7 · 2025: 5 · 2024: 13 · 2023: 11 · 2022: 11 · 2021: 13 · 2020: 14 · 2019: 17 · 2018: 21 · 2017: 19 · 2016: 19 · 2015: 25 · 2014: 23 · 2013: 33 · 2012: 24
- FWCI
- 2.12
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Ageing Research Reviews (publishedVersion)
- PubMed (publishedVersion)
- Funders
- British Heart Foundation (RG/08/009/25841)
- 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 › Geriatrics and Gerontology › Sirtuins and Resveratrol in Medicine
- Keywords
- cellular senescence, senescence biomarkers, replicative senescence, stress-induced premature senescence, oncogene-induced senescence, telomere shortening, DNA damage response, senescence-associated β-galactosidase, senescence-associated heterochromatin foci, PML nuclear bodies, senescence-associated secretory phenotype, age-related diseases, aging
- MeSH terms
- Aging, DNA Damage, Humans, Phenotype, Research, Biomarkers, Telomere, Cellular Senescence, Genomic Instability
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