Replicative senescence revisited.

Marcotte, R.; Wang, E.

doi:10.1093/gerona/57.7.b257

Cited by 86Telomeres, Telomerase, and SenescenceGenetics, Aging, and Longevity in Model OrganismsCancer-related Molecular Pathways

Replicative senescence revisited.

Marcotte, R., Wang, E.·2002·The Journals of Gerontology Series A: Biological Sciences and Medical Sciences

DOI 10.1093/gerona/57.7.b257

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Abstract

Forty years after its discovery, replicative senescence remains a rich source of information about cell-cycle regulation and the progression from a normal to a transformed phenotype. Effectors of this growth-arrested state are being discovered at a great pace. This review discusses the latest findings on the players responsible for establishing replicative senescence, as well as the associated telomere shortening.

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Induction of cellular senescence occurs as a result of extensive replication, which results in telomere shortening or which occurs prematurely after cells are exposed to oxidative, genotoxic, or oncogenic stress.
“Induction of cellular senescence occurs as a result of extensive replication, which results in telomere shortening or which occurs prematurely after cells are exposed to oxidative, genotoxic, or oncogenic stress.27-29”
From Total body irradiation causes long-term mouse BM injury via induction of HSC premature senescence in an Ink4a- and Arf-independent manner (2014) · cites this paper as [28]

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Authors: Marcotte, R., & Wang, E.
Affiliations: Jewish General Hospital (CA)
Corresponding author: Marcotte, R.
Venue: The Journals of Gerontology Series A: Biological Sciences and Medical Sciences
Publisher: Oxford University Press (OUP)
Published: 2002-07-01
Volume: 57
Issue: 7
Pages: B257-B269
ISSN: 1079-5006 (ISSN-L)
1758-535X
DOI: 10.1093/gerona/57.7.b257
OpenAlex: W2137592705
Cited by: 86
References: 183
Citations by year: 2026: 2 · 2025: 1 · 2024: 1 · 2023: 4 · 2022: 13 · 2021: 3 · 2020: 2 · 2019: 3 · 2018: 2 · 2017: 1 · 2016: 4 · 2015: 6 · 2014: 3 · 2013: 5 · 2012: 3
FWCI: 0.61
Type: journal article
Language: en
Open access: closed
Locations: The Journals of Gerontology Series A (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health (5r01ag007444-05)
National Institute on Aging (R01AG 07444)
Topics: Health Sciences › Medicine › Physiology › 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: replicative senescence, cell cycle regulation, telomere shortening, cell transformation, aging
MeSH terms: Animals, Cell Cycle, Humans, Tumor Suppressor Protein p53, Retinoblastoma Protein, Cyclins, Telomere, Cellular Senescence, Cyclin-Dependent Kinase Inhibitor p16, Tumor Suppressor Protein p14ARF, Cyclin-Dependent Kinase Inhibitor p21

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Replicative senescence revisited.

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