Senescent cells: an emerging target for diseases of ageing
Open accessAbstract
Chronological age represents the single greatest risk factor for human disease. One plausible explanation for this correlation is that mechanisms that drive ageing might also promote age-related diseases. Cellular senescence, which is a permanent state of cell cycle arrest induced by cellular stress, has recently emerged as a fundamental ageing mechanism that also contributes to diseases of late life, including cancer, atherosclerosis and osteoarthritis. Therapeutic strategies that safely interfere with the detrimental effects of cellular senescence, such as the selective elimination of senescent cells (SNCs) or the disruption of the SNC secretome, are gaining significant attention, with several programmes now nearing human clinical studies.
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In cancer, the SASP can frequently promote therapy resistance and recurrence.
“In cancer, the SASP can frequently promote therapy resistance and recurrence [34].”
From The role of cellular senescence and SASP in tumour microenvironment (2023) · cites this paper as [34]
In “SASP neutralization” (page not provided), the paper says that suppressing the SASP in a mouse lymphoma model blunts immune surveillance and drives treatment resistance and relapse—the opposite direction from the claim. “SNCs possess a bioactive secretome” describes the SASP as potentially tumour-promoting, but does not say it frequently promotes therapy resistance or recurrence. (LLM, conf=0.85)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredSenescent cells accumulate in most tissues with age and are important components of the overall aging process.
“While senescence has beneficial functions (such as tumor suppression), senescent cells accumulate in most tissues with age, and they are important components of the overall aging process62.”
From The role of retrotransposable elements in ageing and age-associated diseases (2021) · cites this paper as [62]
The Abstract says senescent cells accumulate over time and are directly linked to features of natural ageing. The Discovery and detection of SNCs section describes them in numerous aged rodent and primate tissues, but the passages do not establish the stronger claim that they accumulate in most tissues. (LLM, conf=0.83)
Experimental — accuracy not yet measuredSeveral senolytic drugs, such as ABT-737, BET inhibitors and dasatinib plus quercetin, can selectively induce cell death in senescent cells and effectively improve some symptoms of age-related disease, including cancer, by attenuating SASP factor production.
“Several senolytic drugs, such as ABT‐737, BET inhibitors and dasatinib plus quercetin, can selectively induce cell death in senescent cells and effectively improve some symptoms of age‐related disease, including cancer, by attenuating SASP factor production.81”
From Cellular senescence and senescence-associated secretory phenotype via the cGAS-STING signaling pathway in cancer (2020) · cites this paper as [81]
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredSenescent cells build up in many diseases associated with ageing.
“The literature is becoming inundated with evidence that senescent cells accumulate in a variety of age-associated diseases13.”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [13]
Failsafe cellular senescence occurs in response to oncogene activation, oncosuppressor inactivation, and sublethal insults including telomere shortening, DNA damage, mitochondrial dysfunction, defective/stalled DNA replication, and epigenetic, lysosomal, mechanical, metabolic, mitotic, oxidative, or proteotoxic challenges.
“In particular, this failsafe cellular senescence reportedly occurs in response to (1) potentially carcinogenic events including oncogene activation or oncosuppressor gene inactivation; and (2) several sublethal cellular insults, including telomere shortening, DNA damage, mitochondrial dysfunction, defective/stalled DNA replication and epigenetic, lysosomal, mechanical, metabolic, mitotic, ox”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [958]
Genetic and pharmacological strategies have demonstrated benefits of eliminating senescent cells in aging and disease.
“Genetic and pharmacological strategies have demonstrated the benefits of eliminating senescent cells in the context of aging and disease 10,12,51.”
From Cardiac glycosides are broad-spectrum senolytics (2019) · cites this paper as [51]
Aging and age-related diseases cause senescent cells to build up in many tissues of humans and mice.
“Organismal aging and age-related diseases promote an accumulation of senescent cells in a variety of tissues in both humans and mice (8).”
From Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives (2018) · cites this paper as [8]
Multiple molecules involved in the SASP act as promoters of atherosclerosis and are biomarkers of CVD risk.
“Senescent cells are more than simple bystanders, as multiple molecules involved in the SASP act as promoters of atherosclerosis and are biomarkers of CVD risk.23”
From Senescence-induced inflammation: an important player and key therapeutic target in atherosclerosis (2020) · cites this paper as [23]
Senolytics, small molecules that selectively kill senescent cells, have the potential to prevent and treat various age-related diseases and extend healthspan.
“Small molecules that can selectively kill SCs, termed senolytics, have the potential to prevent and treat a growing number of age-related diseases and extend healthspan2–4.”
From Using proteolysis-targeting chimera technology to reduce navitoclax platelet toxicity and improve its senolytic activity (2020) · cites this paper as [2]
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 [2]
Almost all targeted senolytics are repurposed anticancer agents except the FOXO4-p53 interfering peptide.
“By contrast, almost all the targeted senolytics are repurposed anticancer agents except the FOXO4-p53 interfering peptide2–4.”
From Using proteolysis-targeting chimera technology to reduce navitoclax platelet toxicity and improve its senolytic activity (2020) · cites this paper as [2]
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 [2]
Senescent cells from different cellular origins and tissues show variable sensitivities to different senolytic agents.
“Our studies also confirm some of the previous observations that SCs from different cellular origins and tissues show variable sensitivities to different senolytic agents2–5.”
From Using proteolysis-targeting chimera technology to reduce navitoclax platelet toxicity and improve its senolytic activity (2020) · cites this paper as [2]
Different senescent cells can use different anti-apoptotic pathways (SCAPs) to resist apoptosis.
“This observation is in agreement with the suggestion that different SCs can use different anti-apoptotic pathways (SCAPs) to resist apoptosis2–5.”
From Using proteolysis-targeting chimera technology to reduce navitoclax platelet toxicity and improve its senolytic activity (2020) · cites this paper as [2]
Cell senescence occurs throughout the lifespan but plays a larger role with aging and is postulated to contribute to many diseases of aging including vascular disease, arthritis, and neurodegeneration.
“Cell senescence occurs throughout the lifespan but plays a larger role with aging and is postulated to contribute to many diseases of aging including vascular disease, arthritis, and neurodegeneration. 38”
From Alzheimer’s disease drug development pipeline: 2021 (2021) · cites this paper as [38]
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 [14]
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 [14]
Senolytic drugs identified to date were not discovered by a truly unbiased high-throughput screening method and appear to have limitations in clinical applications.
“However, the senolytic drugs identified to date were not discovered by a truly unbiased high-throughput screening (HTS) method, and thus appear to have limitations in clinical applications15,17–19.”
From A BET family protein degrader provokes senolysis by targeting NHEJ and autophagy in senescent cells (2020) · cites this paper as [15]
The combination of dasatinib and quercetin exhibited remarkable cell-type specificity.
“the combination of dasatinib and quercetin (D + Q), another previously reported senolytic drug20, apparently exhibited remarkable cell-type specificity15”
From A BET family protein degrader provokes senolysis by targeting NHEJ and autophagy in senescent cells (2020) · cites this paper as [15]
In a phase II study of ABT263 for advanced and recurrent small-cell lung carcinoma, transient thrombocytopenia and neutropenia were reported as side-effects.
“in a phase II study of ABT263 (a specific inhibitor of the anti-apoptotic proteins BCL2 and BCL-xL)19 for the treatment of advanced and recurrent small-cell lung carcinoma patients, transient thrombocytopenia and neutropenia were reported as side-effects15.”
From A BET family protein degrader provokes senolysis by targeting NHEJ and autophagy in senescent cells (2020) · cites this paper as [15]
Cellular senescence drives chronic low-grade inflammation, exacerbating aging.
“Cellular senescence impairs the ability of tissue regeneration and drives chronic low-grade inflammation, which exacerbates the aging process.5,6”
From Elimination of senescent cells by β-galactosidase-targeted prodrug attenuates inflammation and restores physical function in aged mice (2020) · cites this paper as [6]
Cellular senescence impairs tissue regeneration.
“Cellular senescence impairs the ability of tissue regeneration and drives chronic low-grade inflammation, which exacerbates the aging process.5,6”
From Elimination of senescent cells by β-galactosidase-targeted prodrug attenuates inflammation and restores physical function in aged mice (2020) · cites this paper as [6]
Senescence is one of the major drivers of aging and clearing senescent cells is a promising approach to treat age-related diseases and improve physical function.
“These studies demonstrated that senescence is one of the major drivers of aging and that clearing senescent cells is a promising approach to treat age-related diseases and improve physical function.6,10”
From Elimination of senescent cells by β-galactosidase-targeted prodrug attenuates inflammation and restores physical function in aged mice (2020) · cites this paper as [6]
Senolytic drugs have significant limitations in killing senescent cells in terms of specificity and broad-spectrum activity because of the dynamic and highly heterogeneous nature of the senescence program.
“However, senolytic drugs have significant limitations in killing senescent cells in terms of specificity and broad-spectrum activity because of the dynamic and highly heterogeneous nature of the senescence program, which leads to the varying sensitivity of different types of senescent cells to current senolytic drugs.6,16,17”
From Elimination of senescent cells by β-galactosidase-targeted prodrug attenuates inflammation and restores physical function in aged mice (2020) · cites this paper as [6]
SASP contributes to local and systemic low-grade inflammation during aging, age-related degenerative phenotypes, and impairment of physical function.
“SASP contributes to local and systemic low-grade inflammation during aging, to age-related degenerative phenotypes, and to impairment of physical function.5,6,43”
From Elimination of senescent cells by β-galactosidase-targeted prodrug attenuates inflammation and restores physical function in aged mice (2020) · cites this paper as [6]
Senescent cells accumulate with age and in many diseases, potentially contributing to pathology.
“Senescent cells produce a distinct inflammatory secretome and have been found to accumulate with age and in many diseases; potentially contributing to pathology [17–21].”
From Untangling senescent and damage‐associated microglia in the aging and diseased brain (2023) · cites this paper as [17]
Senescent cells produce a distinct inflammatory secretome.
“Senescent cells produce a distinct inflammatory secretome and have been found to accumulate with age and in many diseases; potentially contributing to pathology [17–21].”
From Untangling senescent and damage‐associated microglia in the aging and diseased brain (2023) · cites this paper as [17]
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- Authors
- Childs, B. G., Gluscevic, M., Baker, D. J., Laberge, R.-M., Marquess, D., Dananberg, J., & van Deursen, J. M.
- Affiliations
- Mayo Clinic (US)
- Unity Biotechnology (United States) (US)
- Venue
- Nature Reviews Drug Discovery
- Published
- 2017-07-21
- Volume
- 16
- Issue
- 10
- Pages
- 718-735
- ISSN
- 1474-1776 (ISSN-L)
- 1474-1784
- PMC
- PMC5942225
- OpenAlex
- W2739438570
- Cited by
- 1,284
- References
- 216
- Citations by year
- 2026: 146 · 2025: 157 · 2024: 166 · 2023: 162 · 2022: 149 · 2021: 168 · 2020: 146 · 2019: 108 · 2018: 73 · 2017: 8 · 2013: 1
- FWCI
- 11.24
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Reviews Drug Discovery (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Radboud Repository (Radboud University) (submittedVersion)
- Funders
- National Institute on Aging (T32AG049672)
- National Cancer Institute (R01CA168709, 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, senescent cells, aging, age-related diseases, cancer, atherosclerosis, osteoarthritis, senolytics, senescence-associated secretory phenotype, cell cycle arrest, cellular stress, senolytic therapy
- MeSH terms
- Aging, Animals, Humans, Neoplasms, Cellular Senescence, Cell Proliferation, Atherosclerosis, Cell Cycle Checkpoints
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