Cellular Senescence: Aging, Cancer, and Injury
Open accessAbstract
Cellular senescence is a permanent state of cell cycle arrest that occurs in proliferating cells subjected to different stresses. Senescence is, therefore, a cellular defense mechanism that prevents the cells to acquire an unnecessary damage. The senescent state is accompanied by a failure to re-enter the cell cycle in response to mitogenic stimuli, an enhanced secretory phenotype and resistance to cell death. Senescence takes place in several tissues during different physiological and pathological processes such as tissue remodeling, injury, cancer, and aging. Although senescence is one of the causative processes of aging and it is responsible of aging-related disorders, senescent cells can also play a positive role. In embryogenesis and tissue remodeling, senescent cells are required for the proper development of the embryo and tissue repair. In cancer, senescence works as a potent barrier to prevent tumorigenesis. Therefore, the identification and characterization of key features of senescence, the induction of senescence in cancer cells, or the elimination of senescent cells by pharmacological interventions in aging tissues is gaining consideration in several fields of research. Here, we describe the known key features of senescence, the cell-autonomous, and noncell-autonomous regulators of senescence, and we attempt to discuss the functional role of this fundamental process in different contexts in light of the development of novel therapeutic targets.
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Senescent cells contribute to a wide range of age-related pathologies.
“they have been valuable in showing that senescent cells contribute to a wide range of agerelated pathologies”
From Cellular Senescence: Defining a Path Forward (2019) · cites this paper as Calcinotto et al., 2019
Accumulation of senescent cells is causally linked to functional decline in aging tissues.
“Accumulation of senescent cells is causally linked to functional decline in aging tissues.”
From Spatial transcriptomic landscape unveils immunoglobin-associated senescence as a hallmark of aging (2024) · cites this paper as [24]
Quiescent cells can resume proliferation in response to appropriate signals such as growth factors or mitogenic signals, whereas senescent cells cannot.
“Another crucial difference is that quiescent cells can resume proliferation in response to appropriate signals such as stimulation by growth factors or mitogenic signals whereas senescent cells cannot (Campisi and D’Adda Di Fagagna, 2007; Calcinotto et al., 2019; Gorgoulis et al., 2019; Mohamad Kamal et al., 2020).”
From Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021) · cites this paper as Calcinotto et al., 2019
Natural accumulation of senescent cells in mammals during ageing contributes to development of various age-associated diseases.
“The natural accumulation of senescent cells in mammals during ageing contributes to the development of various age‐associated diseases (Baker et al, 2016; Calcinotto et al, 2019; Borghesan et al, 2020).”
From The struggle of a good friend getting old: cellular senescence in viral responses and therapy (2021) · cites this paper as Calcinotto et al, 2019
Chronic senescence is triggered by feedback loops when the senescent stimulus is prolonged, and may cause diseases such as atherosclerosis, arthritis, neurodegenerative disease, and diabetes as well as age-related decline in tissue function.
“Chronic senescence is triggered by feedback loops when the senescent stimulus is prolonged, and may cause diseases such as atherosclerosis, arthritis, neurodegenerative disease, and diabetes [13] as well as effecting classical age-related decline in tissue function [14].”
From Senescence and Cancer: A Review of Clinical Implications of Senescence and Senotherapies (2020) · cites this paper as [13]
When senescent cells persist, their SASP profile becomes damaging and can transform senescent fibroblasts into pro-inflammatory cells, thereby promoting tumour progression.
“However, when senescent cells persist, their SASP profile becomes damaging, and this can transform senescent fibroblasts into pro-inflammatory cells, thereby promoting tumour progression [2,3].”
From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [2]
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Backgroundp53-dependent release of Alarmin HMGB1 is a central mediator of senescent phenotypes
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BackgroundDanazol Treatment for Telomere Diseases
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“Danazol is a synthetic steroid molecule that has telomereelongating capacity and has been used to antagonize accelerated telomere attrition (320).”
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“IFN can also induce senescence by triggering DNA damage in the target cells (232, 312).”
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Cellular Senescence: Defining a Path Forward
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Self-citationMechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype
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Diversity and biology of cancer-associated fibroblasts
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How the ageing microenvironment influences tumour progression
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Aging of the cells: Insight into cellular senescence and detection Methods.
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Research Advances in How the cGAS-STING Pathway Controls the Cellular Inflammatory Response
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A Senescence-Centric View of Aging: Implications for Longevity and Disease
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Self-citationSenescence and Cancer: A Review of Clinical Implications of Senescence and Senotherapies
Wyld, L., Bellantuono, I., Tchkonia, T., Morgan, J., Turner, O., Foss, F., George, J., Danson, S., & Kirkland, J. L. (2020) · Cancers · doi:10.3390/cancers12082134 · Cited by 235 · see citing works
“Chronic senescence is triggered by feedback loops when the senescent stimulus is prolonged, and may cause diseases such as atherosclerosis, arthritis, neurodegenerative disease, and diabetes [13] as well as effecting classical age-related decline in tissue function [14].”
BackgroundAlgorithmic assessment of cellular senescence in experimental and clinical specimens
Kohli, J., Wang, B., Brandenburg, S. M., Basisty, N., Evangelou, K., Varela-Eirin, M., Campisi, J., Schilling, B., Gorgoulis, V., & Demaria, M. (2021) · Nature Protocols · doi:10.1038/s41596-021-00505-5 · Cited by 196 · see citing works
Self-citationCell Senescence, DNA Damage, and Metabolism
Shmulevich, R., & Krizhanovsky, V. (2021) · Antioxidants & Redox Signaling · doi:10.1089/ars.2020.8043 · Cited by 157 · see citing works
Spatial transcriptomic landscape unveils immunoglobin-associated senescence as a hallmark of aging
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The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence
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Eliminating Senescent Cells Can Promote Pulmonary Hypertension Development and Progression
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Oligodendrocyte progenitor cells in Alzheimer's disease: from physiology to pathology
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Senescent hepatic stellate cells promote liver regeneration through IL-6 and ligands of CXCR2
Cheng, N., Kim, K.-H., & Lau, L. F. (2022) · JCI Insight · doi:10.1172/jci.insight.158207 · Cited by 87 · see citing works
“Discussion The accumulation of senescent cells can profoundly influence the aging process, the efficacy of tissue repair, and the pathology of diseases including cancer (12, 64).”
Cellular Senescence as a Therapeutic Target for Age-Related Diseases: A Review
Amaya-Montoya, M., Pérez-Londoño, A., Guatibonza-García, V., Vargas-Villanueva, A., & Mendivil, C. O. (2020) · Advances in Therapy · doi:10.1007/s12325-020-01287-0 · Cited by 82 · see citing works
Targeting senescent cells improves functional recovery after spinal cord injury
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Increased cellular senescence in doxorubicin-induced murine ovarian injury: effect of senolytics
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The struggle of a good friend getting old: cellular senescence in viral responses and therapy
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“INTRODUCTION Aging is one of the major risk factors for many diseases [1], and the development of methods to intervene in aging will significantly reduce the risk of a series of age-related diseases such as cardiovascular and cerebrovascular diseases [2, 3], cancer [4], and Alzheimer’s disease [5].”
BackgroundSenopathies-Diseases Associated with Cellular Senescence
Lushchak, O., Schosserer, M., & Grillari, J. (2023) · Biomolecules · doi:10.3390/biom13060966 · Cited by 35 · see citing works
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Cellular senescence in normal and adverse pregnancy
Farfán-Labonne, B., Leff-Gelman, P., Pellón-Díaz, G., & Camacho-Arroyo, I. (2023) · Reproductive Biology · doi:10.1016/j.repbio.2023.100734 · Cited by 19 · see citing works
Early ageing after cytotoxic treatment for testicular cancer and cellular senescence: Time to act
Lubberts, S., Meijer, C., Demaria, M., & Gietema, J. A. (2020) · Critical Reviews in Oncology/Hematology · doi:10.1016/j.critrevonc.2020.102963 · Cited by 19 · see citing works
Self-citationThe New Frontier of Ageing: Innovations and Insights in Gerontology
Tohit, N. F. M., & Haque, M. (2024) · Advances in Human Biology · doi:10.4103/aihb.aihb_110_24 · Cited by 8 · see citing works
Overview of molecular signatures of senescence and associated resources: pros and cons
Ntintas, O. A., Vagena, S., Pantelis, P., Theocharous, G., Petty, R., Evangelou, K., & Gorgoulis, V. G. (2026) · FEBS Open Bio · doi:10.1002/2211-5463.70134 · Cited by 6 · see citing works
- Authors
- Calcinotto, A., Kohli, J., Zagato, E., Pellegrini, L., Demaria, M., & Alimonti, A.
- Affiliations
- University Medical Center Groningen (NL)
- Venue
- Physiological Reviews
- Publisher
- American Physiological Society
- Published
- 2019-04-01
- Volume
- 99
- Issue
- 2
- Pages
- 1047-1078
- ISSN
- 0031-9333 (ISSN-L)
- 1522-1210
- OpenAlex
- W2908922892
- Semantic Scholar
- 0f14990d81f31932eaf095dc809aa48eb03a1307
- Cited by
- 1,270
- References
- 374
- Citations by year
- 2026: 136 · 2025: 212 · 2024: 272 · 2023: 233 · 2022: 211 · 2021: 109 · 2020: 80 · 2019: 16
- FWCI
- 12.28
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Physiological Reviews (publishedVersion)
- PubMed (publishedVersion)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (submittedVersion, other-oa)
- SERVAL (Université de Lausanne) (submittedVersion)
- Padua Research Archive (University of Padova) (submittedVersion)
- Funders
- ERC consolidator (683136)
- Swiss Cancer League (KFS4267-08-2017)
- Dr. Joseph Steiner Foundation
- Swiss Card-Onco-Grant of Alfred and Annemarie von Sick
- SNSF (310030_176045)
- IBSA Foundation
- KWF Kankerbestrijding (Dutch Cancer Society) (10989/2017-1)
- 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, cancer, tissue damage, cell cycle arrest, senescence-associated secretory phenotype, tissue remodeling, embryonic development, senescence induction, senolytics, cancer prevention
- MeSH terms
- Aging, Animals, Cell Transformation, Neoplastic, Humans, Neoplasms, Wound Healing, Cellular Senescence, Cell Proliferation
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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