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Linking functional decline of telomeres, mitochondria and stem cells during ageing
Open accessAbstract
The study of human genetic disorders and mutant mouse models has provided evidence that genome maintenance mechanisms, DNA damage signalling and metabolic regulation cooperate to drive the ageing process. In particular, age-associated telomere damage, diminution of telomere 'capping' function and associated p53 activation have emerged as prime instigators of a functional decline of tissue stem cells and of mitochondrial dysfunction that adversely affect renewal and bioenergetic support in diverse tissues. Constructing a model of how telomeres, stem cells and mitochondria interact with key molecules governing genome integrity, 'stemness' and metabolism provides a framework for how diverse factors contribute to ageing and age-related disorders.
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“telomerase activity and recombination‐based processes that maintain telomere length are critical for tissue homeostasis (Sahin & Depinho, 2010).”
From P66SHC deletion improves fertility and progeric phenotype of late-generation TERC-deficient mice but not their short lifespan (2016) · cites this paper as Sahin & Depinho, 2010
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“Telomere dysfunction is a primary hallmark of aging, causing molecular and cellular damage and serving as a driver or amplifier of the molecular circuitries driving the aging process and associated diseases.1,2,7”
From TERT activation targets DNA methylation and multiple aging hallmarks (2024) · cites this paper as [7]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Telomere dysfunction has been causally implicated as a rate-limiting pathogenetic step in age-related diseases including premature aging (progeroid) syndromes, cardiovascular diseases, inflammatory bowel disease, pulmonary fibrosis, metabolic diseases and neurological diseases.2,7,8”
From TERT activation targets DNA methylation and multiple aging hallmarks (2024) · cites this paper as [7]
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“Of particular relevance to this study, age-progressive loss of telomere function in mice has been shown to provoke widespread p53 activation resulting in activation of cellular checkpoints of apoptosis, impaired proliferation and senescence, compromised tissue stem cell and progenitor function, marked tissue atrophy and physiological impairment in many organ systems 1 , 6 .”
From Telomerase reactivation reverses tissue degeneration in aged telomerase-deficient mice (2011) · cites this paper as [1]
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“Telomere loss and uncapping provokes progressive tissue atrophy, stem cell depletion, organ system failure, and impaired tissue injury responses 1 .”
From Telomerase reactivation reverses tissue degeneration in aged telomerase-deficient mice (2011) · cites this paper as [1]
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“Telomere dysfunction is itself an aging hallmark and can also contribute to other hallmarks such as genome instability, stem cell exhaustion, mitochondrial dysfunction and cellular senescence.2,7”
From TERT activation targets DNA methylation and multiple aging hallmarks (2024) · cites this paper as [7]
The cited source says what the claim attributes to it.
In the citing paper
“Telomeres, specialized chromatin structures that preserve chromosomal integrity, undergo progressive attrition during aging-associated tissue renewal, leading to loss of their capping function.”
From TERT activation targets DNA methylation and multiple aging hallmarks (2024) · cites this paper as [7]
In the citing paper
“The ageing immune system is characterised by a decline in stem cells, alterations in T-lymphocyte production, blunting of the B-cell led antibody response and reduced phagocytic activity of neutrophils, macrophages and natural killer cells (50, 51).”
From Frailty in elderly people (2013) · cites this paper as [50]
In the citing paper
“This senescent immune system may function adequately in the quiescent state but fail to respond appropriately to the stress of acute inflammation (50).”
From Frailty in elderly people (2013) · cites this paper as [50]
In the citing paper
“DNA damage in association with telomere dysfunction and shortening precipitates premature aging and shortened lifespan, leading to depletion of almost all tissue stem cell reserves and dysfunction of stem cells, including self-renewal and repair capacity of ESCs and melanocytes of the follicle during the hair growth process [113, 114].”
From Ultraviolet Radiation‐Induced Skin Aging: The Role of DNA Damage and Oxidative Stress in Epidermal Stem Cell Damage Mediated Skin Aging (2016) · cites this paper as [113]
In the citing paper
“Thus, repeated cell division may result in progressive telomere shortening that in turn results in DNA damage that can no longer be repaired efficiently due to agerelated defects in DNA repair mechanisms (75).”
From Causes, consequences, and reversal of immune system aging (2013) · cites this paper as [75]
In the citing paper
“The analysis of stem and progenitor cells from various tissues has revealed that aging often results in the dysregulation of similar molecular pathways (75).”
From Causes, consequences, and reversal of immune system aging (2013) · cites this paper as [75]
In the citing paper
“in HSCs and neural stem cells (NSCs) of mice, excessive cellular ROS concentrations lead to abnormal proliferation, malignancy and compromised stem cell self-renewal11–14”
From Stem cell aging: mechanisms, regulators and therapeutic opportunities (2014) · cites this paper as [12]
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Metadata
- Authors
- Sahin, E., & DePinho, R. A.
- Affiliations
- Harvard University (US)
- Venue
- Nature
- Published
- 2010-03
- Volume
- 464
- Issue
- 7288
- Pages
- 520-528
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC3733214
- OpenAlex
- W1988354925
- Cited by
- 759
- References
- 100
- Citations by year
- 2026: 15 · 2025: 31 · 2024: 43 · 2023: 38 · 2022: 34 · 2021: 41 · 2020: 34 · 2019: 38 · 2018: 39 · 2017: 42 · 2016: 48 · 2015: 54 · 2014: 53 · 2013: 55 · 2012: 83
- FWCI
- 7.97
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- National Cancer Institute (U01CA84313, U01CA084313, R01CA84628, R01CA084628)
- 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
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- aging, telomeres, telomere dysfunction, telomere capping, p53 activation, DNA damage signaling, genome maintenance, mitochondrial dysfunction, tissue stem cells, stemness, bioenergetics, metabolic regulation, age-related diseases
- MeSH terms
- Aging, Animals, Hematopoietic System, Homeostasis, Humans, Mitochondria, Phenotype, Stem Cells, Tumor Suppressor Protein p53, Telomere, Genome, Telomerase
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