The DOI matches its Crossref record; 216 of the 216 references it cites were found in a registry or an index.
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 the citing paper
“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]
Checked by a reasoning model — may be wrong.
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
“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]
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
“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]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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 the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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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Citations
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The limited in vitro lifetime of human diploid cell strains
Hayflick, L. (1965) · Experimental Cell Research · doi:10.1016/0014-4827(65)90211-9 · Cited by 5,876
Lawrence, R. C., Felson, D. T., Helmick, C. G., Arnold, L. M., Choi, H. K., Deyo, R. A., Gabriel, S. E., Hirsch, R., Hochberg, M. C., Hunder, G. G., et al. (2007) · Arthritis & Rheumatism · doi:10.1002/art.23176 · Cited by 5,599
Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a
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Cellular senescence: when bad things happen to good cells
Campisi, J., & d'Adda di Fagagna, F. (2007) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2233 · Cited by 4,441
Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders
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Chronic Health Conditions in Adult Survivors of Childhood Cancer
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Aging, Cellular Senescence, and Cancer
Campisi, J. (2013) · Annual Review of Physiology · doi:10.1146/annurev-physiol-030212-183653 · Cited by 2,954
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Reactive astrocyte nomenclature, definitions, and future directions
Escartin, C., Galea, E., Lakatos, A., O’Callaghan, J. P., Petzold, G. C., Serrano-Pozo, A., Steinhäuser, C., Volterra, A., Carmignoto, G., Agarwal, A., et al. (2021) · Nature Neuroscience · doi:10.1038/s41593-020-00783-4 · Cited by 2,513
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Cellular senescence in ageing: from mechanisms to therapeutic opportunities
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Metadata
- 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
- 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
- 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, 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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