Cellular senescence in aging and age-related disease: from mechanisms to therapy
Open accessAbstract
Cellular senescence, a process that imposes permanent proliferative arrest on cells in response to various stressors, has emerged as a potentially important contributor to aging and age-related disease, and it is an attractive target for therapeutic exploitation. A wealth of information about senescence in cultured cells has been acquired over the past half century; however, senescence in living organisms is poorly understood, largely because of technical limitations relating to the identification and characterization of senescent cells in tissues and organs. Furthermore, newly recognized beneficial signaling functions of senescence suggest that indiscriminately targeting senescent cells or modulating their secretome for anti-aging therapy may have negative consequences. Here we discuss current progress and challenges in understanding the stressors that induce senescence in vivo, the cell types that are prone to senesce, and the autocrine and paracrine properties of senescent cells in the contexts of aging and age-related diseases as well as disease therapy.
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Even in whole tissues with a small senescent cell fraction (1-3%), some core signature genes can be identified as differentially regulated.
“These findings suggest that even in whole tissues where the number of senescent cells is small (most aged or diseased tissues contained 1%–3% senescent cells [33]), some of the genes of our core signature can be identified as differentially regulated.”
From Unmasking Transcriptional Heterogeneity in Senescent Cells (2017) · cites this paper as [33]
The citation is attached to the parenthetical claim about the proportion of senescent cells, not to the citing authors’ finding about core-signature genes. The source’s “Senescence in normal aging” section (page unavailable) describes senescent cells as rare in aged tissues, but our copy does not give the claimed 1%–3% figure for most aged or diseased tissues. (LLM, conf=0.84)
Experimental — accuracy not yet measuredThe SASP composition and strength varies substantially, depending on the duration of senescence, origin of the pro-senescence stimulus, and cell type.
“The SASP composition and strength varies substantially, depending on the duration of senescence, origin of the pro-senescence stimulus, and cell type (Childs et al., 2015).”
From Cellular Senescence: Defining a Path Forward (2019) · cites this paper as Childs et al., 2015
In “Origin and identification of senescent cells in vivo,” the paper says the SASP could vary with time spent in senescence, the nature of the stress, and cell type. It presents this as a prediction rather than an established finding that the composition and strength vary substantially; it does report differing SASP profiles in two mouse models. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThe role of senescence in human disease is clear from cellular studies, while in vivo evidence is only now catching up.
“The role of senescence in human disease is clear from cellular studies, while in vivo evidence is only now catching up”
From Cellular Senescence: Defining a Path Forward (2019) · cites this paper as Childs et al., 2015
The Abstract contrasts a wealth of knowledge from cultured cells with a poor understanding of senescence in living organisms, supporting the claim that in vivo evidence lags. But it calls senescence only a potentially important contributor to age-related disease, and the Senescence in normal aging section says in vitro evidence suggests mechanisms rather than establishing a clear role in human disease. The indexed passages provide section labels but no page numbers. (LLM, conf=0.88)
Experimental — accuracy not yet measuredEvidence links senescence to other common age-associated human diseases including neurodegenerative disorders, glaucoma, cataract, atherosclerosis and cardiovascular disease, diabetes, osteoarthritis, pulmonary, and renal and liver fibrosis.
“Evidence linking senescence to other common age-associated human diseases has recently emerged. These diseases include neurodegenerative disorders, glaucoma, cataract, atherosclerosis and cardiovascular disease, diabetes, osteoarthritis, pulmonary, and renal and liver fibrosis”
From Cellular Senescence: Defining a Path Forward (2019) · cites this paper as Childs et al., 2015
The “Senescence in age-related disease” section (page unavailable) links senescence to glaucoma, cataracts, atherosclerosis, diabetes, osteoarthritis, and pulmonary and liver fibrosis; the “Aging and atherosclerosis” section also discusses cardiovascular disease. The passages found do not establish the claimed links to neurodegenerative disorders or renal fibrosis. The paper also says senescent cells restrict, rather than drive, liver fibrosis, and cautions that senescence at sites of pathology may be a consequence rather than a cause. (LLM, conf=0.88)
Experimental — accuracy not yet measuredSenescent cells contribute to aging and age-related pathologies through SASP.
“Senescent cells contribute to aging and age-related pathologies21,22,23 through their senescence-associated secretory phenotype (SASP).24,25,26”
From Uncovering the signatures of aging and senescence in the human dorsolateral prefrontal cortex (2026) · cites this paper as [23]
Senescent cell accumulation via aging-induced epigenetic, proteotoxic and genotoxic stresses usually has a causal role in many age-related diseases, including glaucoma, cataracts, diabetes mellitus, and osteoarthritis.
“Furthermore, senescent cell accumulation via aging-induced epigenetic, proteotoxic and genotoxic stresses usually exhibits a causal role in many age-related diseases, including glaucoma, cataracts, diabetes mellitus, osteoarthritis, among others (Childs et al. 2015).”
From Benefits of Metformin in Attenuating the Hallmarks of Aging (2020) · cites this paper as Childs et al. 2015
Cells can resume proliferation upon resolution of stress.
“Cells can resume proliferation upon resolution of the stress (Childs et al., 2015).”
From Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021) · cites this paper as Childs et al., 2015
Accumulation of senescent cells in ageing organisms contributes to many diseases, including cancer.
“The accumulation of senescent cells in ageing organisms contributes to many diseases, including cancer 46.”
From Cardiac glycosides are broad-spectrum senolytics (2019) · cites this paper as [46]
In vivo, the best currently available models for senescent cell detection are reporter-harbouring transgenic mice (p16-LUC, p16 tdTom) and transgenic mouse strains used for selective senescent cell removal (INK-ATTAC, p16-3MR).
“In vivo, the best currently available models for senescent cell detection are reporter-harbouring transgenic mice (p16-LUC, p16 tdTom)199,200 and transgenic mouse strains used for selective senescent cell removal (INK-ATTAC, p16-3MR).201”
From Senescence-induced inflammation: an important player and key therapeutic target in atherosclerosis (2020) · cites this paper as [201]
Ageing is a significant risk factor for type 2 diabetes.
“Ageing is a significant risk factor for T2DM36”
From Exercise activates AMPK in mouse and human pancreatic islets to decrease senescence (2024) · cites this paper as [36]
Senescent cells accumulate with age and as a result of exposure to a variety of stressors including radiation.
“SCs accumulate with age and as a result of the exposure to a variety of stressors including radiation.”
From Using proteolysis-targeting chimera technology to reduce navitoclax platelet toxicity and improve its senolytic activity (2020) · cites this paper as [1]
Senescent cells play a causal role in many age-related diseases via expression of the senescence-associated secretory phenotype to secrete inflammatory mediators and proteases.
“They play a causal role in many age-related diseases (such as neurodegenerative and cardiovascular diseases, osteoarthritis, and cancer) via expression of the senescence-associated secretory phenotype (SASP) to secret various inflammatory mediators and proteases1–7.”
From Using proteolysis-targeting chimera technology to reduce navitoclax platelet toxicity and improve its senolytic activity (2020) · cites this paper as [1]
Senescent cells that are irreversibly cell-cycle arrested accumulate in many tissues during normal aging.
“In many tissues, irreversibly cell cycle-arrested senescent cells accumulate during normal aging.”
From Aging of hematopoietic stem cells (2018) · cites this paper as [56]
In healthy aging, common cellular stresses can yield primary senescent cells that diminish tissue-repair capacity due to cell cycle arrest in progenitor cells and increase production of proinflammatory and matrix-degrading molecules.
“In healthy aging, common cellular stresses can yield primary senescent cells that diminish tissue-repair capacity due to cell cycle arrest in progenitor cells and increase production of proinflammatory and matrix-degrading molecules (3, 4).”
From Aging and Lung Disease (2020) · cites this paper as [3]
Natural lung aging is associated with molecular and physiological changes that cause alterations in lung function, diminished pulmonary remodeling and regenerative capacity, and increased susceptibility to acute and chronic lung diseases.
“Natural lung aging is associated with molecular and physiological changes that cause alterations in lung function, diminished pulmonary remodeling and regenerative capacity, and increased susceptibility to acute and chronic lung diseases.”
From Aging and Lung Disease (2020) · cites this paper as [3]
Exposure to extrinsic time-related effects such as chronic atmospheric pollution, dusts, particulates, and gases induces low-level insults to cellular function and accelerates aging of the lung.
“Exposure to extrinsic time-related effects, such as chronic exposure to atmospheric pollution, dusts, particulates, and gases, induce low-level insults to cellular function and accelerate aging of the lung (3).”
From Aging and Lung Disease (2020) · cites this paper as [3]
Age-associated changes in intrinsic mechanisms that aid cell regeneration and repair, such as depletion of adult stem cell reservoirs, mitochondrial dysfunction, increased oxidative stress, and telomere shortening, contribute to an inability of lung cells to maintain baseline homeostasis.
“Age-associated changes in intrinsic mechanisms that aid in cell regeneration and repair, such as depletion of adult stem cell reservoirs, mitochondrial dysfunction, increased oxidative stress, and telomere shortening, contribute to an inability of lung cells to maintain baseline homeostasis.”
From Aging and Lung Disease (2020) · cites this paper as [3]
Senescent cells display a genetic and morphologic phenotype distinct from growth-competent cells and can have a detrimental impact on neighboring cells, structural components, and composition of the extracellular matrix.
“Senescent cells display a genetic and morphologic phenotype that is distinct from growth-competent cells and can have a detrimental impact on neighboring cells, structural components, and composition of the extracellular matrix (ECM) (3).”
From Aging and Lung Disease (2020) · cites this paper as [3]
Excessive accumulation of senescent cells in numerous tissues leads to multiple chronic diseases, tissue dysfunction, age-related diseases and organ ageing.
“Excessive accumulation of senescent cells in numerous tissues leads to multiple chronic diseases, tissue dysfunction, age-related diseases and organ ageing.”
From Immune Clearance of Senescent Cells to Combat Ageing and Chronic Diseases (2020) · cites this paper as [12]
Excessive accumulation of senescent cells causally shortens the healthy lifespan and drives organ ageing, age-related organ deterioration/disorders, tissue dysfunction and chronic diseases, including cardiovascular diseases, cancer, neurodegenerative diseases and osteoarthritis.
“However, excessive accumulation of senescent cells causally shortens the healthy lifespan [11] and drives organ ageing [12], age-related organ deterioration/disorders [13,14], tissue dysfunction and chronic diseases, including cardiovascular diseases (CVDs) [15,16], cancer [2], neurodegenerative diseases [17,18] and osteoarthritis [19].”
From Immune Clearance of Senescent Cells to Combat Ageing and Chronic Diseases (2020) · cites this paper as [12]
An age-associated increase in NK cell senescence has been shown to impair antiviral immune responses in response to influenza.
“An age-associated increase in NK cell senescence has been shown to impair antiviral immune responses in response to influenza (3, 128).”
From Aging and Lung Disease (2020) · cites this paper as [3]
Age-associated impairments in innate and adaptive immune responses in the lung may contribute to increased susceptibility of older persons developing an asthma exacerbation.
“Age-associated impairments in innate and adaptive immune responses in the lung may contribute to increased susceptibility of older persons developing an asthma exacerbation (3, 19, 107, 109, 110).”
From Aging and Lung Disease (2020) · cites this paper as [3]
Age-associated changes in genomic instability, telomere shortening, epigenetic alterations, cellular senescence, impaired autophagy, and mitochondrial dysfunction may promote IPF development and progression.
“Further, age-associated changes in genomic instability, telomere shortening, epigenetic alterations, cellular senescence, impaired autophagy, and mitochondrial dysfunction may promote IPF development and progression (3, 12, 62, 84, 88, 89, 116, 145).”
From Aging and Lung Disease (2020) · cites this paper as [3]
Age-associated immunosenescence and cellular senescence in response to exposure to cigarette smoke can greatly impact COPD pathogenesis.
“Age-associated immunosenescence and cellular senescence in response to exposure to cigarette smoke can greatly impact COPD pathogenesis (3, 19, 86).”
From Aging and Lung Disease (2020) · cites this paper as [3]
Age-associated alterations in immune surveillance, specifically decreased innate and adaptive immune responses, and dysfunctional immune response regulation can be responsible for increased lung pathology in response to infectious stimuli.
“Age-associated alterations in immune surveillance, specifically decreased innate and adaptive immune responses, and dysfunctional immune response regulation can be responsible for increased lung pathology in response to infectious stimuli (3, 62, 106, 110, 114, 135).”
From Aging and Lung Disease (2020) · cites this paper as [3]
Cellular senescence contributes to aging and age-related diseases and is a target of therapeutic interventions.
“Cellular senescence, a process that essentially entails permanent proliferative arrest of cells in response to various stressors, has emerged as a potentially important contributor to aging and age-related diseases and hence is a target of therapeutic interventions (3).”
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 [3]
Removal of senescent cells promotes healthy aging in mice.
“Importantly, removal of senescent cells promotes healthy aging in mice, making senescence‐associated inflammatory signaling an attractive target of therapeutic intervention for aging and age‐related disease (Tilstra et al, 2012; Childs et al, 2015; Baker et al, 2016; Ogrodnik et al, 2021).”
From Mechanisms of DNA damage-mediated neurotoxicity in neurodegenerative disease (2022) · cites this paper as Childs et al, 2015
SA-β-gal in diverse types of senescent cells is a widely used marker for identifying senescence in vitro and in vivo, linked to increased lysosome content.
“Notably, SA-β-gal in diverse types of senescent cells is one widely used marker for identifying senescence in vitro and in vivo, which is linked to the increased content of lysosomes.20–23”
From Elimination of senescent cells by β-galactosidase-targeted prodrug attenuates inflammation and restores physical function in aged mice (2020) · cites this paper as [20]
SA-β-gal is widely used as a marker of cellular senescence.
“While SA-β-gal is widely used as a marker of cellular senescence,20–22”
From Elimination of senescent cells by β-galactosidase-targeted prodrug attenuates inflammation and restores physical function in aged mice (2020) · cites this paper as [20]
Senescence is heterogeneous: a variety of insults may incite senescence, the inflammatory secretory phenotype is modified depending on cell type, and the senescent phenotype may change based on the stage of senescence.
“A challenge in targeting senescence is the apparent heterogeneity of this cellular state, wherein a variety of insults may incite senescence, the inflammatory secretory phenotype is modified depending on cell type, and the senescent phenotype may even change based on the stage of senescence [22–24].”
From Untangling senescent and damage‐associated microglia in the aging and diseased brain (2023) · cites this paper as [23]
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- [152]Baker DJ Opposing roles for p16Ink4a and p19Arf in senescence and ageing caused by BubR1 insufficiency Nat. Cell Biol 2008 10 825 836 18516091 PMC2594014
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- Authors
- Childs, B. G., Durik, M., Baker, D. J., & van Deursen, J. M.
- Affiliations
- Mayo Clinic (US)
- Venue
- Nature Medicine
- Published
- 2015-12
- Volume
- 21
- Issue
- 12
- Pages
- 1424-1435
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- PMC
- PMC4748967
- OpenAlex
- W2193792657
- Cited by
- 2,363
- References
- 170
- Citations by year
- 2026: 257 · 2025: 278 · 2024: 275 · 2023: 278 · 2022: 259 · 2021: 266 · 2020: 246 · 2019: 191 · 2018: 153 · 2017: 106 · 2016: 51 · 2015: 1 · 2012: 1
- FWCI
- 12.68
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Radboud Repository (Radboud University) (submittedVersion)
- Funders
- National Institute on Aging (AG41122-01P2, P01AG041122, R37AG013925)
- National Cancer Institute (R01CA166347, R01CA096985)
- 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, age-related diseases, senescent cells, senescence induction, senolytics, anti-aging therapy, paracrine signaling, autocrine signaling, proliferative arrest
- MeSH terms
- Aging, Animals, Disease, Health, Humans, Longevity, Signal Transduction, Cellular Senescence
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