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Inflammatory networks during cellular senescence: causes and consequences.
Open accessAbstract
Chronic inflammation is associated with aging and plays a causative role in several age-related diseases such as cancer, atherosclerosis and osteoarthritis. The source of this chronic inflammation is often attributed to the progressive activation of immune cells over time. However, recent studies have shown that the process of cellular senescence, a tumor suppressive stress response that is also associated with aging, entails a striking increase in the secretion of pro-inflammatory proteins and might be an important additional contributor to chronic inflammation. Here, we list the secreted factors that make up the pro-inflammatory phenotype of senescent cells and describe the impact of these factors on tissue homeostasis. We also summarize the cellular pathways/processes that are known to regulate this phenotype – namely, the DNA damage response, microRNAs, key transcription factors and kinases and chromatin remodeling.
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“Finally, the SASP also includes proteins that can help senescent cells evade immune recognition and clearance (92, 93).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [93]
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“Specialized SASP chemokines are able to attract distinct subsets of immune cells, including NK cells, neutrophils, dendritic cells, monocytes/macrophages, B cells and T cells75,151,152.”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [152]
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In the citing paper
“Therefore, prolonged secretion of SASP factors, such as interleukin (IL)‐1β and MMP, could drive cancer development.44, 45, 46”
From Cellular senescence and senescence-associated secretory phenotype via the cGAS-STING signaling pathway in cancer (2020) · cites this paper as [44]
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“The secretion of these and similar proteins by senescent cells is predicted to cause chronic inflammation, at least locally and possibly systemically (91–93, 107).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [93]
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In the citing paper
“many SASP components directly or indirectly promote inflammation (59, 92, 93, 107, 108).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [93]
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“Senescent cells, presumably by virtue of SASP-derived factors, can stimulate the infiltration of leukocytes (93, 131, 132), which produce reactive toxic moieties that can cause DNA damage.”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [93]
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“Notably, Nfkb1 (p50) and Cebpb, two well-known TF coding genes that have been reported to regulate SASP (Freund et al., 2010), were also upregulated in a subset of cells in the lineage 1-2-3-4 (Figure 4C)”
From Single-Cell Transcriptome Analysis Reveals Six Subpopulations Reflecting Distinct Cellular Fates in Senescent Mouse Embryonic Fibroblasts (2020) · cites this paper as Freund et al., 2010
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In the citing paper
“which comprise a negative feedback loop to dampen NF-κB activity (Taganov et al., 2006; Freund et al., 2010).”
From Four faces of cellular senescence (2011) · cites this paper as Freund et al., 2010
In the citing paper
“Components of the SASP, such as interleukin (IL)-6, IL-8, and MCP-1, are increased in obese adults and adolescents and could contribute to such a proinflammatory state, together with effects of macrophages and other mediators of inflammation (31,53,54).”
From Cellular Senescence in Type 2 Diabetes: A Therapeutic Opportunity (2015) · cites this paper as [31]
In the citing paper
“However, NF-κB dependent pro-inflammatory factors are the key components of SASP with IL-6 and IL-8 being the most conserved and robustly expressed cytokines (Hardy et al., 2005; Davalos et al., 2010; Freund et al., 2010; Soto-Gamez and Demaria, 2017).”
From Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021) · cites this paper as Freund et al., 2010
In the citing paper
“The main components of SASP include a plethora of soluble signaling factors, such as, pro-inflammatory cytokines, chemokines, growth modulators, angiogenic factors, proteases, bioactive lipids, extracellular matrix components, and matrix metalloproteinases (MMPs) (Coppé et al., 2010a; Freund et al., 2010; Acosta et al., 2013; Lopes-Paciencia et al., 2019).”
From Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021) · cites this paper as Freund et al., 2010
In the citing paper
“Consistent SASP elements in the majority of senescent cells are IL-1α, IL-1β, IL-6, IL-8, IL-18, and TNF-α,15,105,110 all of which are clinically validated CVD risk factors.1,5”
From Senescence-induced inflammation: an important player and key therapeutic target in atherosclerosis (2020) · cites this paper as [15]
In the citing paper
“As depicted in Figure 3, cellular senescence can be a consequence of two processes which may run in parallel and are intertwined. The first is replicative exhaustion resulting from chronological age or intense proliferation (telomere dependent)20,124,125 and the latter is exposure to cardiovascular risk factors (stress-induced).13–18”
From Senescence-induced inflammation: an important player and key therapeutic target in atherosclerosis (2020) · cites this paper as [15]
In the citing paper
“In turn, senescence may impact on these same pathways via positive or negative feedback loops as well as other intracellular pathways and extracellular processes, such as the immune modulation, inflammation [16], regulation, and maintenance of the extracellular matrix, and angiogenesis [17].”
From Senescence and Cancer: A Review of Clinical Implications of Senescence and Senotherapies (2020) · cites this paper as [16]
In the citing paper
“These cells have short telomeres, high activity of the enzyme galactosidase, show high expression of the DNA repair complex associated protein H2Ax and constitutive activation of p53 and p38 map kinase (p38 MAPK), as well the cyclin inhibitor p16 [9, 27] (Table 1).”
From Senescence of T Lymphocytes: Implications for Enhancing Human Immunity (2016) · cites this paper as [27]
In the citing paper
“Senescent cells themselves secrete a raft of inflammatory mediators, termed the senescence associated secretory phenotype (SASP) (16).”
From The impact of ageing on monocytes and macrophages (2021) · cites this paper as [16]
In the citing paper
“Cellular senescence is thought to further propagate nearby tissue aging through intracellular metabolic compromise (eg, mitochondrial dysfunction) (Sahin et al, 2011) and altered production of secretory factors that promote aging by increasing degradation of nearby tissue and sterile inflammation (Coppe et al, 2010a, b;Freund et al, 2010) (ie, senescence-associated secretory phenotype, SASP).”
From Sleep health: Reciprocal regulation of sleep and innate immunity (2017) · cites this paper as Freund et al, 2010
In the citing paper
“It has been observed that MK2 stabilizes the mRNAs and upregulate the expression of many cytokines”
From Rapamycin inhibits the secretory phenotype of senescent cells by a Nrf2-independent mechanism (2017) · cites this paper as Freund et al., 2010
In the citing paper
“HIV-associated inflammation and/or exposure to nucleoside analogues have been associated with changes in these and other key biologic pathways (33–40).”
From HIV and Aging: State of Knowledge and Areas of Critical Need for Research. A Report to the NIH Office of AIDS Research by the HIV and Aging Working Group (2012) · cites this paper as [38]
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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
Self-citationCellular senescence: from physiology to pathology
Muñoz-Espín, D., & Serrano, M. (2014) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm3823 · Cited by 2,818
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Metadata
- Authors
- Freund, A., Orjalo, A. V., Desprez, P.-Y., & Campisi, J.
- Affiliations
- Buck Institute for Research on Aging (US)
- Corresponding author
- Campisi, Judith
- Venue
- Trends in Molecular Medicine
- Publisher
- Elsevier BV
- Published
- 2010-05
- Volume
- 16
- Issue
- 5
- Pages
- 238-246
- ISSN
- 1471-4914 (ISSN-L)
- PMC
- PMC2879478
- OpenAlex
- W2108273756
- Semantic Scholar
- 8123cb6b710081dd80220a3cd9089f7301c783df
- Cited by
- 1,354
- References
- 77
- Citations by year
- 2026: 62 · 2025: 89 · 2024: 105 · 2023: 92 · 2022: 115 · 2021: 109 · 2020: 110 · 2019: 88 · 2018: 103 · 2017: 88 · 2016: 78 · 2015: 75 · 2014: 69 · 2013: 61 · 2012: 54
- FWCI
- 5.50
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Trends in Molecular Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Science Foundation
- Larry L. Hillblom Foundation
- National Institute for Health and Care Research
- National Institutes of Health
- National Institute on Aging (R56AG009909, AG017242, RL1AG032117, AG-09909, P01AG025901, R37AG009909, P30AG025708, AG032117, AG025708, P01AG017242, AG025901, T32AG000266)
- 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, chronic inflammation, senescence-associated secretory phenotype, aging, age-related diseases, DNA damage response, microRNA, transcription factors, kinases, chromatin remodeling, tissue homeostasis, immune cell activation
- MeSH terms
- Animals, Humans, Inflammation, Models, Biological, Transcription Factors, Cellular Senescence, MicroRNAs
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