A three-state model of telomere control over human proliferative boundaries
Open accessAbstract
Intrinsic limits on cellular proliferation in human somatic tissue serves as a tumor suppressor mechanism by restricting cell growth in aged cells with accrued pre-cancerous mutations. This is accompanied by the potential cost of restricting regenerative capacity and contributing to cellular and organismal aging. Emerging data support a model where telomere erosion controls proliferative boundaries through the progressive change of telomere structure from a protected state, through two distinct states of telomere deprotection. In this model telomeres facilitate a controlled permanent cell cycle arrest with a stable diploid genome during differentiation and may serve as an epigenetic sensor of general stress in DNA metabolism processes.
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Short telomeres retain enough telomere-binding proteins to inhibit DNA repair and avoid fusions, producing a persistent DNA damage signal and permanent proliferative arrest.
“Such short telomeres, however, retain a sufficient number of telomere-binding proteins to inhibit DNA repair and avoid fusions5, and consequently fuel a persistent DNA damage signal that enforces a permanent DNA damage-induced proliferative arrest.”
From Telomere dysfunction in ageing and age-related diseases (2022) · cites this paper as [5]
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References 69 · Cited by 106
- Authors
- Cesare, A. J., & Karlseder, J.
- Affiliations
- Salk Institute for Biological Studies (US)
- Corresponding author
- Karlseder, Jan
- Venue
- Current Opinion in Cell Biology
- Publisher
- Elsevier BV
- Published
- 2012-12
- Volume
- 24
- Issue
- 6
- Pages
- 731-738
- ISSN
- 0955-0674 (ISSN-L)
- PMC
- PMC3532573
- OpenAlex
- W2060209663
- Cited by
- 106
- References
- 69
- Citations by year
- 2026: 7 · 2025: 7 · 2024: 7 · 2023: 5 · 2022: 8 · 2021: 13 · 2020: 6 · 2019: 3 · 2018: 13 · 2017: 7 · 2016: 7 · 2015: 9 · 2014: 8 · 2013: 4 · 2012: 2
- FWCI
- 0.80
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Current Opinion in Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- US National Institutes of Health (NIH) (5T32CA009370-29, GM087476)
- Salk Institute Cancer Center Core Grant (P30 CA014195-38)
- 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
- telomere shortening, cell cycle arrest, tumor suppression, cellular aging, DNA metabolism, telomere structure, differentiation
- MeSH terms
- Animals, Cell Differentiation, Humans, Models, Biological, Neoplasms, Stress, Physiological, Telomere, Cellular Senescence, Cell Proliferation, M Phase Cell Cycle Checkpoints
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