Senescent cells spread the word: non-cell autonomous propagation of cellular senescence
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These inflammatory cytokines promote senescence locally in a paracrine manner and perhaps at a systemic level.
“These inflammatory cytokines promote senescence locally in a paracrine manner30 and perhaps, at a systemic level.111”
From Senescence-induced inflammation: an important player and key therapeutic target in atherosclerosis (2020) · cites this paper as [30]
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Senescence and tumour clearance is triggered by p53 restoration in murine liver carcinomas
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Self-citationA complex secretory program orchestrated by the inflammasome controls paracrine senescence
Acosta, J. C., Banito, A., Wuestefeld, T., Georgilis, A., Janich, P., Morton, J. P., Athineos, D., Kang, T.-W., Lasitschka, F., Andrulis, M., et al. (2013) · Nature Cell Biology · doi:10.1038/ncb2784 · Cited by 2,278 · cited 2× · see citing works
“Adding to our understanding of this process, a recent report by Gil and colleagues showed that the SASP can also mediate paracrine transmission of cellular senescence (Acosta et al , 2013).”
Oncogene-Induced Senescence Relayed by an Interleukin-Dependent Inflammatory Network
Kuilman, T., Michaloglou, C., Vredeveld, L. C. W., Douma, S., van Doorn, R., Desmet, C. J., Aarden, L. A., Mooi, W. J., & Peeper, D. S. (2008) · Cell · doi:10.1016/j.cell.2008.03.039 · Cited by 2,086 · see citing works
Senescence of activated stellate cells limits liver fibrosis
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Self-citationSenescence of Activated Stellate Cells Limits Liver Fibrosis
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Self-citationFour faces of cellular senescence
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“…of p16 and p21 levels on neighbouring immune cells, the functional consequences of which are not yet so clear. enforce cell cycle arrest, modify the microenvironment and trigger immune surveillance of senescent cells (Xue et al , 2007; Krizhanovsky et al , 2008; Rodier and Campisi, 2011).”
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“Similarly, the SASP has been shown to be pro-and anti-tumorigenic depending on the microenvironment (Krtolica et al , 2001; Xue et al , 2007; Lujambio et al , 2013; Figure 1).”
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- Authors
- Tasdemir, N., & Lowe, S. W.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Corresponding author
- Lowe, Scott W
- Venue
- The EMBO Journal
- Published
- 2013-06-18
- Volume
- 32
- Issue
- 14
- Pages
- 1975-1976
- ISSN
- 0261-4189 (ISSN-L)
- 1460-2075
- PMC
- PMC3715860
- OpenAlex
- W2041908350
- Cited by
- 43
- References
- 12
- Citations by year
- 2026: 5 · 2025: 4 · 2024: 6 · 2023: 4 · 2022: 5 · 2021: 1 · 2019: 5 · 2018: 2 · 2017: 2 · 2016: 2 · 2015: 4 · 2014: 3
- FWCI
- 2.09
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- The EMBO Journal (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Cold Spring Harbor Laboratory Institutional Repository (Cold Spring Harbor Laboratory) (submittedVersion)
- Funders
- National Institute on Aging (R01AG016379)
- National Cancer Institute (P30CA008748)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- cellular senescence, paracrine signaling, senescence-associated secretory phenotype, tissue homeostasis, cancer therapy
- MeSH terms
- Animals, Humans, Cellular Senescence, Inflammasomes
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