The DOI matches its Crossref record; 88 of the 88 references it cites were found in a registry or an index.
Impact of senescence-associated secretory phenotype and its potential as a therapeutic target for senescence-associated diseases
Open accessAbstract
"Cellular senescence" is a state in which cells undergo irreversible cell cycle arrest in response to a variety of cellular stresses. Once cells senesce, they are strongly resistant to any mitogens, including oncogenic stimuli. Therefore, cellular senescence has been assumed to be a potent anticancer mechanism. Although irreversible cell-cycle arrest is traditionally considered the major characteristic of senescent cells, recent studies have revealed some additional functions. Most noteworthy is the increased secretion of various secretory proteins, such as inflammatory cytokines, chemokines, growth factors, and MMPs, into the surrounding extracellular fluid. These newly recognized senescent phenotypes, termed senescence-associated secretory phenotypes (SASPs), reportedly contribute to tumor suppression, wound healing, embryonic development, and even tumorigenesis promotion. Thus, SASPs appear to be beneficial or deleterious, depending on the biological context. As senescent cells are known to accumulate during the aging process in vivo, it is quite possible that their accumulation in aged tissues promotes age-associated functional decline and various diseases, including cancers, at least to some extent. Here, we focus on and discuss the functional and regulatory network of SASPs toward opening up new possibilities for controlling aging and aging-associated diseases.
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![Figure 5 Strategies for senescence‐associated secretory phenotype (SASP) attenuation. SASP factors could be blocked by targeting its induction (e.g., nuclear factor‐κB [NF‐κB] inhibitor, mammalian target of rapamycin [mTOR] inhibitor, or bromo and extra terminal domain [BET] inhibitor) or its activity (e.g., interleukin [IL]‐1 receptor antagonist, anti‐IL‐6 receptor antibody, IL‐6 inhibitor, or tumor necrosis factor‐α inhibitor).](/paper-figures/730c811b8cf14d54838fac279ba35097/impact-of-senescence-associated-secretory-phenotype-and-its-potential-as-a-figure-5.jpg)
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“Senescent cells accumulate with age in the dermis and epidermis, which can be accelerated by various harmful factors, such as DNA-damaging agents (eg, x-rays, ultraviolet radiation, and cigarette smoke) and mitochondrial dysfunction.56”
From The costs and benefits of senotherapeutics for human health (2022) · cites this paper as [56]
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1 retracted
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Sorted by citations
Cellular Senescence: Aging, Cancer, and Injury
Calcinotto, A., Kohli, J., Zagato, E., Pellegrini, L., Demaria, M., & Alimonti, A. (2019) · Physiological Reviews · doi:10.1152/physrev.00020.2018 · Cited by 1,270
“They can influence neighboring proliferating cells and the recruitment and activation of immune cells in aging tissues and tumors (92, 339), as is detailed in sect.”
BackgroundAge and Age-Related Diseases: Role of Inflammation Triggers and Cytokines
Rea, I. M., Gibson, D. S., McGilligan, V., McNerlan, S. E., Alexander, H. D., & Ross, O. A. (2018) · Frontiers in Immunology · doi:10.3389/fimmu.2018.00586 · Cited by 1,267
“There appears to be multi-level control of senescence and the SASP secretome, which includes the tumor suppressor pathways involved in the cell cycle arrest and the NF-κB and persistent damage response (DAMP) pathway, involved in triggering transcription of the SASP-related factors (115).”
BackgroundExploiting senescence for the treatment of cancer
Wang, L., Lankhorst, L., & Bernards, R. (2022) · Nature Reviews Cancer · doi:10.1038/s41568-022-00450-9 · Cited by 867
Unmasking senescence: context-dependent effects of SASP in cancer
Faget, D. V., Ren, Q., & Stewart, S. A. (2019) · Nature Reviews Cancer · doi:10.1038/s41568-019-0156-2 · Cited by 863
Skeletal Muscle as Potential Central Link between Sarcopenia and Immune Senescence
Nelke, C., Dziewas, R., Minnerup, J., Meuth, S. G., & Ruck, T. (2019) · eBioMedicine · doi:10.1016/j.ebiom.2019.10.034 · Cited by 437
Metadata
- Authors
- Watanabe, S., Kawamoto, S., Ohtani, N., & Hara, E.
- Affiliations
- Research Institute for Microbial Diseases, The University of Osaka (JP)
- Tokyo University of Science (JP)
- Japanese Foundation For Cancer Research (JP)
- Corresponding author
- Watanabe, Sugiko
- Venue
- Cancer Science
- Publisher
- Wiley
- Published
- 2017-04
- Volume
- 108
- Issue
- 4
- Pages
- 563-569
- ISSN
- 1347-9032 (ISSN-L)
- 1349-7006
- PMC
- PMC5406532
- OpenAlex
- W2587299332
- Cited by
- 321
- References
- 88
- Citations by year
- 2026: 22 · 2025: 27 · 2024: 29 · 2023: 39 · 2022: 33 · 2021: 41 · 2020: 47 · 2019: 47 · 2018: 33 · 2017: 3
- FWCI
- 4.36
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cancer Science (publishedVersion, cc-by-nc-nd)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Funders
- Astellas Foundation for Research on Metabolic Disorders
- Naito Foundation
- Japan Agency for Medical Research and Development
- 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
- senescence-associated secretory phenotype, cellular senescence, aging, senolytics, secreted proteins, inflammatory cytokines, chemokines, matrix metalloproteinases, tumor suppression, carcinogenesis, cell cycle arrest, therapeutic target
- MeSH terms
- Aging, Animals, Cell Transformation, Neoplastic, Disease, Humans, Neoplasms, Phenotype, Cellular Senescence, Secretory Pathway, Cell Cycle Checkpoints
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