Roles of telomere biology in cell senescence, replicative and chronological ageing
Open accessAbstract
Telomeres with G-rich repetitive DNA and particular proteins as special heterochromatin structures at the termini of eukaryotic chromosomes are tightly maintained to safeguard genetic integrity and functionality. Telomerase as a specialized reverse transcriptase uses its intrinsic RNA template to lengthen telomeric G-rich strand in yeast and human cells. Cells sense telomere length shortening and respond with cell cycle arrest at a certain size of telomeres referring to the “Hayflick limit.” In addition to regulating the cell replicative senescence, telomere biology plays a fundamental role in regulating the chronological post-mitotic cell ageing. In this review, we summarize the current understandings of telomere regulation of cell replicative and chronological ageing in the pioneer model system Saccharomyces cerevisiae and provide an overview on telomere regulation of animal lifespans. We focus on the mechanisms of survivals by telomere elongation, DNA damage response and environmental factors in the absence of telomerase maintenance of telomeres in the yeast and mammals.
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Replicative senescence occurs due to telomere shortening, activation of cell-cycle checkpoints (p53/p21 WAF1 and p16 Ink4A/RB pathways), and accumulation of oxidative or genotoxic stress.
“This occurs due to telomere shortening (Liu et al. 2019), activation of cellcycle checkpoints (e.g.p53/p21 WAF1 and p16 Ink4A /RB pathways) (Han and Kim 2023), and accumulation of oxidative or genotoxic stress (Yu et al. 2018).”
From Primary cell cultures versus immortalized cell lines: critical comparative insights into biological fidelity and translational applications (2026) · cites this paper as Liu et al. 2019
Cellular senescence is a major mechanism of aging at the cellular level, though likely not the only one.
“Cellular senescence has been described as a major mechanism for aging at the cellular level, although likely not the only mechanism.”
From Reducing Senescent Cell Burden in Aging and Disease (2020) · cites this paper as [16]
Multiple inducers of cellular senescence include DNA damage, reactive metabolites, inflammation, oncogenes, mitogens, proteotoxic stress, and damage-associated molecular patterns.
“There are multiple inducers of cellular senescence, including DNA damage, reactive metabolites, inflammation, oncogenes, mitogens, proteotoxic stress, and damage-associated molecular patterns [16–18].”
From Reducing Senescent Cell Burden in Aging and Disease (2020) · cites this paper as [16]
Cellular senescence is a primary aging process and tumor suppressive mechanism with features including irreversible growth arrest, apoptosis resistance, SASP, mitochondrial dysfunction, and DNA/chromatin changes.
“Cellular senescence is a primary aging process and tumor suppressive mechanism characterized by irreversible growth arrest, apoptosis resistance, production of a senescence-associated secretory phenotype (SASP), mitochondrial dysfunction, and alterations in DNA and chromatin.”
From Reducing Senescent Cell Burden in Aging and Disease (2020) · cites this paper as [16]
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- Authors
- Liu, J., Wang, L., Wang, Z., & Liu, J.-P.
- Affiliations
- Hangzhou Normal University (CN)
- Institute of Ageing Research, School of Medicine, Hangzhou Normal University, Hangzhou 311121, Zhejiang, China
- Corresponding author
- Liu, Jun
- Venue
- Cells
- Publisher
- MDPI AG
- Published
- 2019-01-15
- Volume
- 8
- Issue
- 1
- Pages
- 54
- ISSN
- 2073-4409 (ISSN-L)
- PMC
- PMC6356700
- OpenAlex
- W2910427173
- Cited by
- 164
- References
- 89
- Citations by year
- 2026: 15 · 2025: 11 · 2024: 25 · 2023: 21 · 2022: 29 · 2021: 38 · 2020: 19 · 2019: 6
- FWCI
- 2.70
- Type
- journal article
- Language
- en
- Open access
- gold
- dx.doi.org
- Licence
- Locations
- Cells (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, other-oa)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Natural Science Foundation of China (31501110, 81530039)
- Chinese Academy of Sciences
- Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
- China Postdoctoral Science Foundation (2014M551470)
- Hangzhou Normal University
- Directorate for Biological Sciences
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Structure and Function
- Keywords
- telomeres, telomere biology, replicative senescence, chronological aging, telomerase, telomere shortening, Hayflick limit, cell cycle arrest, DNA damage response, telomere maintenance, lifespan, Saccharomyces cerevisiae, heterochromatin, telomere elongation
- MeSH terms
- Animals, DNA Repair, Humans, Longevity, Models, Biological, Saccharomyces cerevisiae, Telomere, Cellular Senescence, Mice, Telomere Homeostasis, Telomere Shortening
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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