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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Cellular senescence is an evolutionarily conserved state of stable replicative arrest induced by pro-ageing stressors implicated in IPF pathogenesis.
“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]
The Abstract and 'Senescence is a multi-step evolving process' describe growth arrest, including a transition to stable cell-cycle arrest. 'Causes and effector pathways of senescence' identifies telomere erosion, DNA lesions, reactive oxygen species and proteotoxic stress as senescence-related stressors. The cited passages do not establish that senescence is evolutionarily conserved or that these stressors are implicated in IPF pathogenesis; the paper also distinguishes replicative senescence from other forms of senescence. (LLM, conf=0.86)
Experimental — accuracy not yet measuredSenescent cells paracrinely promote proliferation and tissue deterioration through secretion of the SASP.
“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]
In “Senescence is a multi-step evolving process” (page unavailable), the paper says SASP-mediated paracrine signalling affects cell proliferation. In “Senescence in ageing and age-related disease” (page unavailable), it says SASP components are thought to promote proliferation of neoplastic cells and may intensify age-related tissue deterioration. The citing sentence presents those qualified effects as established and general. (LLM, conf=0.86)
Experimental — accuracy not yet measuredInhibition of STING in cells and human tissue can block the inflammatory response of senescent cells.
“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]
The section ‘Senescence is a multi-step evolving process’ says senescent cells commonly produce proinflammatory factors and can induce local inflammation. But ‘Senescence in ageing and age-related disease’ calls their contribution to chronic inflammation during ageing an untested idea, so the source does not establish that they are major contributors. The citation is attached to that description of senescent cells, not to the citing authors’ STING-inhibition result. (LLM, conf=0.88)
Experimental — accuracy not yet measuredBoth proliferating and post-mitotic cells can be induced to senescence.
“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]
The “Senescence of post-mitotic cells” section (page not provided) reports senescence-associated properties in post-mitotic neurons and senescence-like features in adipocytes. It treats post-mitotic senescence as a developing possibility rather than establishing that these cells can be induced to senescence; by contrast, the “Causes and effector pathways” section describes induction of senescence in proliferating cells. (LLM, conf=0.86)
Experimental — accuracy not yet measuredSenescent cells accumulate in many vertebrate tissues with age and contribute to age-related pathologies, presumably through their secretion of factors constituting the senescence-associated secretory phenotype.
“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]
Senescence is triggered by telomere shortening, DNA damage, oxidative stress, and oncogenic signals.
“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]
Senescent cells have been implicated in the etiology of aging.
“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]
Senescent cells accumulate inside the body during aging.
“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]
Most studies analyze senescent phenotypes 7-10 days after applying senescence inducers.
“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]
The section ‘Senescence is a multi-step evolving process’ says cultured cells usually reach senescence within several weeks of exposure to stressors, but does not say when studies analyze their phenotypes. Searches for 7–10 days and assessment timing found no passage establishing the claimed practice. (LLM, conf=0.73)
Experimental — accuracy not yet measuredWhen AP was administered during wound closure, healing was delayed with similar kinetics as 4- or 18-month-old ATTAC mice without prior AP treatment.
“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]
The 'Senescence in ageing and age-related disease' section says AP20187 was used to eliminate senescent cells in INK-ATTAC mice. The 'Acute versus chronic senescence' section discusses senescence during wound closure, but neither section reports AP administration during wound closure, delayed healing, or a comparison with untreated 4- or 18-month-old mice. Pages were not provided in our copy. (LLM, conf=0.76)
Experimental — accuracy not yet measuredThe cGAS-STING pathway regulates cellular senescence.
“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]
The 'Causes and effector pathways of senescence' section discusses several pathways that induce senescence, but does not mention cGAS–STING. Searches for cGAS–STING and its expanded name found no passage in our copy linking that pathway to regulation of senescence. (LLM, conf=0.76)
Experimental — accuracy not yet measuredSenescence is a highly dynamic, multi-step process in which properties of senescent cells continuously evolve and diversify in a context-dependent manner.
“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
Senescent cells accumulate during organismal aging due to increased generation and inefficient clearance.
“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]
Cellular senescence driven by telomere dysfunction is a causal driver of ageing and age-related pathology.
“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
Cellular senescence plays a crucial role in brain aging, neurodegeneration, and dementia through the SASP, which represents a major source of inflammation.
“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]
Senescence may 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.
“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]
Many types of chemotherapy cause DNA damage, 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.
“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]
Senescent cells accumulate during aging, causing chronic inflammation.
“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
Accumulation of senescent cells is associated with ageing of tissues.
“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]
Secretion of chemoattractants including IL-8 and MIP-1 recruits immune cells to ageing tissue.
“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]
Senescent cells accumulate with age throughout the body and eventually promote tissue deterioration, producing a low-grade chronic inflammatory context and acquiring a phenotype that prevents their clearance.
“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]
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.
“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]
Accumulation of senescent cells in tissues contributes to age-related diseases.
“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]
PPARα ligands selectively eliminate senescent chondrocytes via cell death through apoptosis.
“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]
Cellular senescence plays a crucial role in aging and age-related diseases.
“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]
Cellular senescence accumulates in aged organisms.
“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]
Senescent cells accumulated in different tissues of aged mice, consistent with observation that SA-β-gal-positive cells increased in aged livers, kidneys and lungs.
“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]
Senescent cells accumulate with age, neurodegenerative disease and cognitive decline, neuropsychiatric disorders, and after TBI.
“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]
Senescent MEFs remain viable and can be metabolically active in culture for many months.
“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]
Activation of the senescence programme leads to cellular and molecular changes such as proliferation arrest, chromatin remodelling, elevated expression of cell cycle inhibitors, activation of a DNA damage response, enlargement of the lysosomal compartment, and activation of SASP.
“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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- 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
- 100
- 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
- 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 › 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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