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The role of senescent cells in ageing
Open accessAbstract
Cellular senescence has historically been viewed as an irreversible cell-cycle arrest mechanism that acts to protect against cancer, but recent discoveries have extended its known role to complex biological processes such as development, tissue repair, ageing and age-related disorders. New insights indicate that, unlike a static endpoint, senescence represents a series of progressive and phenotypically diverse cellular states acquired after the initial growth arrest. A deeper understanding of the molecular mechanisms underlying the multi-step progression of senescence and the development and function of acute versus chronic senescent cells may lead to new therapeutic strategies for age-related pathologies and extend healthy lifespan.
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In the citing paper
“Cellular senescence is an evolutionarily conserved state of stable replicative arrest induced by pro-ageing stressors also implicated in IPF pathogenesis, including telomere attrition, oxidative stress, DNA damage and proteome instability.”
From Cellular senescence mediates fibrotic pulmonary disease (2017) · cites this paper as [8]
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
“Through secretion of the senescence-associated secretory phenotype (SASP), a broad repertoire of cytokines, chemokines, matrix remodelling proteases and growth factors, senescent cells paracrinely promote proliferation and tissue deterioration8.”
From Cellular senescence mediates fibrotic pulmonary disease (2017) · cites this paper as [8]
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
“These data establish that inhibition of STING, both in cells and in human tissue, can block the inflammatory response of senescent cells—major contributors to inflammation during ageing8.”
From cGAS–STING drives ageing-related inflammation and neurodegeneration (2023) · cites this paper as [8]
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
“Both proliferating and post-mitotic cells (e.g., fully differentiated cells) can be induced to senescence,3,4”
From Single-cell senescence identification reveals senescence heterogeneity, trajectory, and modulators (2024) · cites this paper as [4]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Senescent cells (SnCs) accumulate in many vertebrate tissues with age and contribute to age-related pathologies1–3, presumably through their secretion of factors contributing to the senescence-associated secretory phenotype (SASP)4–6.”
From Local clearance of senescent cells attenuates the development of post-traumatic osteoarthritis and creates a pro-regenerative environment (2017) · cites this paper as [2]
The cited source says what the claim attributes to it.
In the citing paper
“Senescent cells accumulated in different tissues of aged mice,4,40,41 which was consistent with our observation that SA-β-gal-positive cells increased in aged livers, kidneys and lungs (Supplementary information, Fig. S5a–c).”
From Elimination of senescent cells by β-galactosidase-targeted prodrug attenuates inflammation and restores physical function in aged mice (2020) · cites this paper as [4]
The cited source says what the claim attributes to it.
In the citing paper
“Senescence is triggered by stressors such as telomere shortening, DNA damage, oxidative stress, and oncogenic signals5,6,7,8”
From Cellular senescence in human liver under normal aging and cancer (2026) · cites this paper as [8]
The cited source says what the claim attributes to it.
In the citing paper
“Senescent cells, which have been implicated in the etiology of aging35”
From SIRT6 represses LINE1 retrotransposons by ribosylating KAP1 but this repression fails with stress and age (2014) · cites this paper as [35]
The cited source says what the claim attributes to it.
In the citing paper
“Senescent cells accumulate inside the body during aging4,8”
From Single-cell senescence identification reveals senescence heterogeneity, trajectory, and modulators (2024) · cites this paper as [4]
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In the citing paper
“However, most studies analyze senescent phenotypes 7–10 days after applying the senescence inducers [36, 37].”
From Unmasking Transcriptional Heterogeneity in Senescent Cells (2017) · cites this paper as [37]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“When AP was administered during wound closure, healing was delayed with similar kinetics as 4- or 18-month-old ATTAC mice without prior AP treatment, indicating that acute senescence mechanisms are preserved with aging and not influenced by constitutive clearance of senescent cells 3 .”
From Naturally occurring p16Ink4a-positive cells shorten healthy lifespan (2016) · cites this paper as [3]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“We and others have previously described a role of the cGAS–STING pathway in the regulation of cellular senescence—a hallmark of ageing5–8.”
From cGAS–STING drives ageing-related inflammation and neurodegeneration (2023) · cites this paper as [8]
Experimental — accuracy not yet measuredIn the citing paper
“Senescence is considered to be a highly dynamic, multi-step process, during which the properties of senescent cells continuously evolve and diversify in a context dependent manner.”
From Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021) · cites this paper as Van Deursen, 2014
In the citing paper
“Mounting evidence, however, indicates that senescent cells accumulate during organismal aging due to their increased generation coupled to inefficient clearance [935, 941, 960, 961].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [935]
In the citing paper
“cellular senescence, driven by telomere dysfunction, has been shown to be a causal driver of ageing and age-related pathology (van Deursen, 2014).”
From Telomeres and cell senescence—size matters not (2017) · cites this paper as van Deursen, 2014
In the citing paper
“Among these aging hallmarks, cellular senescence plays a crucial role in brain aging, neurodegeneration, and dementia 36 through the SASP, which represents a major source of inflammation. 37”
From Senescence, brain inflammation, and oligomeric tau drive cognitive decline in Alzheimer's disease: Evidence from clinical and preclinical studies (2024) · cites this paper as [37]
In the citing paper
“It may also be a key effector mechanism of many types of anticancer therapies, such as chemotherapy, radiotherapy, and endocrine therapies, both directly and via bioactive molecules released by senescent cells that may stimulate an immune response.”
From Senescence and Cancer: A Review of Clinical Implications of Senescence and Senotherapies (2020) · cites this paper as [52]
In the citing paper
“Many types of chemotherapy cause DNA damage (DNA strand breaks or cross linking), which can, if severe, cause cell death via the DNA damage response, or they may trigger a non-lethal DDR, leading to acute or chronic senescence, depending on the extent and duration of the stimulus [52].”
From Senescence and Cancer: A Review of Clinical Implications of Senescence and Senotherapies (2020) · cites this paper as [52]
In the citing paper
“As senescent cells accumulate during aging, causing chronic inflammation (van Deursen, 2014)”
From Integrin Beta 3 Regulates Cellular Senescence by Activating the TGF-β Pathway (2017) · cites this paper as van Deursen, 2014
In the citing paper
“While the limit to the extent of proliferation of cells that have damaged DNA is considered to be a natural defense against malignancy, the accumulation of senescent cells is associated with the ageing of tissues [17, 18].”
From Senescence of T Lymphocytes: Implications for Enhancing Human Immunity (2016) · cites this paper as [18]
In the citing paper
“In addition, the secretion of chemoattractants including IL-8 and MIP-1 recruit immune cells to ageing tissue [18]”
From Senescence of T Lymphocytes: Implications for Enhancing Human Immunity (2016) · cites this paper as [18]
In the citing paper
“Senescent cells accumulate with age throughout the body and, although playing a protective role by preventing the appearance of cancer cells, they eventually promote tissue deterioration, producing a low-grade but chronic inflammatory context and acquiring a phenotype that prevents their clearance from the tissue in which they reside [14, 114].”
From Senescence-related impairment of autophagy induces toxic intraneuronal amyloid-β accumulation in a mouse model of amyloid pathology (2023) · cites this paper as [114]
In the citing paper
“Mounting evidence from human samples and preclinical animal models shows that the excessive presence of senescent cells is a contributing cause of ageing, which is featured by a functional decline in multiple physiological systems [39,40].”
From Immune Clearance of Senescent Cells to Combat Ageing and Chronic Diseases (2020) · cites this paper as [39]
In the citing paper
“Accumulation of senescent cells in tissues contributes to age-related diseases [[3], [4], [5], [6], [7]].”
From Fibrates as drugs with senolytic and autophagic activity for osteoarthritis therapy (2019) · cites this paper as [4]
In the citing paper
“Our results demonstrate that PPARα ligands selectively eliminate senescent chondrocytes via cell death through apoptosis [4].”
From Fibrates as drugs with senolytic and autophagic activity for osteoarthritis therapy (2019) · cites this paper as [4]
In the citing paper
“It is widely accepted that cellular senescence plays a crucial role in aging and age-related diseases (36).”
From Senolytic Combination of Dasatinib and Quercetin Alleviates Intestinal Senescence and Inflammation and Modulates the Gut Microbiome in Aged Mice (2021) · cites this paper as [36]
In the citing paper
“One major hallmark of aging is the chronic accumulation of cellular senescence, a permanent state of cell-cycle arrest in response to various damaging stimuli.3,4”
From Elimination of senescent cells by β-galactosidase-targeted prodrug attenuates inflammation and restores physical function in aged mice (2020) · cites this paper as [4]
In the citing paper
“Senescent cells accumulate with age [23, 157, 175], neurodegenerative disease and cognitive decline [15], neuropsychiatric disorders [33], and have recently been discovered to accumulate after TBI [3, 123, 131, 132, 151].”
From Early onset senescence and cognitive impairment in a murine model of repeated mTBI (2021) · cites this paper as [157]
In the citing paper
“Senescent MEFs remain viable (Fig. S1B) and can be metabolically active in culture for many months [2].”
From Iron accumulation in senescent cells is coupled with impaired ferritinophagy and inhibition of ferroptosis (2018) · cites this paper as [2]
In the citing paper
“Activation of the senescence programme leads to cellular and molecular changes such as proliferation arrest, chromatin remodelling, elevated expression of cell cycle inhibitors (such as p16INK4A or p21CIP1), activation of a DNA damage response, enlargement of the lysosomal compartment, and activation of a senescence-associated secretory phenotype (SASP).5,6”
From Paracrine roles of cellular senescence in promoting tumourigenesis (2018) · cites this paper as [6]
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Metadata
- Authors
- van Deursen, J. M.
- Venue
- Nature
- Published
- 2014-05-21
- Volume
- 509
- Issue
- 7501
- Pages
- 439-446
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC4214092
- OpenAlex
- W2130458932
- Cited by
- 2,623
- References
- 99
- Citations by year
- 2026: 160 · 2025: 217 · 2024: 251 · 2023: 295 · 2022: 285 · 2021: 364 · 2020: 272 · 2019: 203 · 2018: 195 · 2017: 132 · 2016: 140 · 2015: 83 · 2014: 24
- FWCI
- 14.84
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Radboud Repository (Radboud University) (submittedVersion)
- Funders
- Foundation for the National Institutes of Health
- Glenn Foundation for Medical Research
- National Institute on Aging (AG41122-01P2, P01AG041122)
- National Cancer Institute (R01CA166347, R01CA096985, R01CA96985)
- 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
- Health Sciences › Medicine › Geriatrics and Gerontology › Sirtuins and Resveratrol in Medicine
- Keywords
- cellular senescence, aging, senolytics, age-related diseases, tissue repair, cancer prevention, growth arrest, healthspan, senolytic therapy
- MeSH terms
- Aging, Animals, Disease, Humans, Longevity, Mitosis, Models, Biological, Cellular Senescence
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