Telomeres: history, health, and hallmarks of aging
Open accessAbstract
The escalating social and economic burden of an aging world population has placed aging research at center stage. The hallmarks of aging comprise diverse molecular mechanisms and cellular systems that are interrelated and act in concert to drive the aging process. Here, through the lens of telomere biology, we examine how telomere dysfunction may amplify or drive molecular biological processes underlying each hallmark of aging and contribute to development of age-related diseases such as neurodegeneration and cancer. The intimate link of telomeres to aging hallmarks informs preventive and therapeutic interventions designed to attenuate aging itself and reduce the incidence of age-associated diseases.
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tDDR activation and TAF accumulation are often causally connected to other ageing-associated processes including mitochondrial dysfunction, altered nutrient sensing, impaired autophagy, loss of proteostasis and epigenetic dysregulation, suggesting a telomere-centric rationale for many ageing hallmarks.
“tDDR activation and TAF accumulation are often causally connected to other ageing-associated processes. These include mitochondrial dysfunction, altered nutrient sensing, impaired autophagy, loss of proteostasis and epigenetic dysregulation, which suggests that there is a unifying ‘telomere-centric’ mechanistic rationale for many ageing hallmarks, as also proposed in ref.29.”
From Telomere dysfunction in ageing and age-related diseases (2022) · cites this paper as [29]
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- Authors
- Chakravarti, D., LaBella, K. A., & DePinho, R. A.
- Affiliations
- The University of Texas MD Anderson Cancer Center (US)
- Corresponding author
- DePinho, Ronald A.
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2021-01
- Volume
- 184
- Issue
- 2
- Pages
- 306-322
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC8081271
- OpenAlex
- W3119985674
- Cited by
- 637
- References
- 152
- Citations by year
- 2026: 84 · 2025: 141 · 2024: 173 · 2023: 124 · 2022: 82 · 2021: 31 · 2013: 1
- FWCI
- 13.74
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (R01 CA084628, UL1TR003167, TL1TR003169)
- National Center for Advancing Translational 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, hallmarks of aging, telomere dysfunction, aging, age-related diseases, neurodegeneration, cancer, anti-aging interventions
- MeSH terms
- Aging, Animals, Health, Humans, Telomere, Cellular Senescence, Telomerase, Genomic Instability
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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