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The Senescence-Associated Secretory Phenotype: The Dark Side of Tumor Suppression
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Cellular senescence is a tumor-suppressive mechanism that permanently arrests cells at risk for malignant transformation. However, accumulating evidence shows that senescent cells can have deleterious effects on the tissue microenvironment. The most significant of these effects is the acquisition of a senescence-associated secretory phenotype (SASP) that turns senescent fibroblasts into proinflammatory cells that have the ability to promote tumor progression.
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In the citing paper
“In 30–70% of senescent cells, this SASP entails pro-inflammatory, proapoptotic and pro-fibrotic factors7,31,40,59–64, some of which can cause previously non-senescent cells to become senescent both locally and at a distance in an endocrine manner24,39,47.”
From Cellular senescence and senolytics: the path to the clinic (2022) · cites this paper as [60]
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
“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 [92]
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
“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 [92]
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
“we observed an elevation of SA-β-gal activity, an increase in classical markers of cellular senescence (including p21/CDKN1A, GDF15 and IL8 mRNAs) and a reduction in LMNB1 mRNA, all consistent with a senescent phenotype”
From Single-cell and spatial transcriptomics map senescent vascular cells in arterial remodeling during atherosclerosis in mice (2025) · cites this paper as [32]
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
“Further, the SASP can recruit immature immune-suppressive myeloid cells to prostate and liver tumors (Di Mitri et al., 2014; Eggert et al., 2016) and stimulate tumorigenesis by driving angiogenesis and metastasis (Coppe ´ et al., 2010).”
From Cellular Senescence: Defining a Path Forward (2019) · cites this paper as Coppe et al., 2010
Experimental — accuracy not yet measured
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In the citing paper
“we generated a gene set (SenMayo) consisting of 125 previously identified senescence/SASP-associated factors”
From A new gene set identifies senescent cells and predicts senescence-associated pathways across tissues (2022) · cites this paper as [81]
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
“factors secreted by senescent cells may directly or indirectly promote chronic inflammation that is thought to be a major factor in many, if not all, age-related diseases (2, 9, 10).”
From The DNA damage response induces inflammation and senescence by inhibiting autophagy of GATA4. (2015) · cites this paper as [9]
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
“Furthermore, senescent cells secrete bioactive mediators, including degradative enzymes, inflammatory cytokines and growth factors, which may further drive stem cell dysfunction with aging127.”
From Stem cell aging: mechanisms, regulators and therapeutic opportunities (2014) · cites this paper as [127]
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
“increased mitochondrial load/dysfunction and reactive oxygen species”
From Evolution of the immune system in humans from infancy to old age (2015) · cites this paper as [99]
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
“The SASP is composed of pro-inflammatory cytokines, chemokines, exosomes, growth factors, and extracellular matrix-degrading proteins that are released into the surrounding tissue environment following the induction of growth arrest.24,25,26,27,28,29”
From Uncovering the signatures of aging and senescence in the human dorsolateral prefrontal cortex (2026) · cites this paper as [24]
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
“The SASP has also been shown to have paracrine activities, inducing senescence in nearby cells.24”
From Uncovering the signatures of aging and senescence in the human dorsolateral prefrontal cortex (2026) · cites this paper as [24]
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
“Control of the secretome in senescent cells is achieved at many levels, from transcriptional regulation to autocrine feedback loops, but persistent DDR appears to be critical for regulation of the SASP (Coppé et al. 2010).”
From Cellular senescence and its effector programs (2014) · cites this paper as Coppé et al. 2010
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
“Thus, the development of the SASP is largely dependent on a persistent DDR associated with senescence stimuli (Coppé et al. 2010).”
From Cellular senescence and its effector programs (2014) · cites this paper as Coppé et al. 2010
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“The SASP of senescent cells is not static; it can change over time78–80 and varies depending on the type of cells that became senescent and how senescence was induced16,44,59,60,81.”
From Cellular senescence and senolytics: the path to the clinic (2022) · cites this paper as [60]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
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 [92]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Sncs are often metabolically very active with a robust secretome [senescence-associated secretory phenotype (SASP)] (7).”
From Senolytic Drugs: Reducing Senescent Cell Viability to Extend Health Span (2021) · cites this paper as [7]
The cited source says what the claim attributes to it.
In the citing paper
“Senescent cells secrete a plethora of factors, including pro-inflammatory cytokines and chemokines, growth modulators, angiogenic factors, and matrix metalloproteinases (MMPs), collectively termed the senescent associated secretory phenotype (SASP) or senescence messaging secretome (SMS) (Figure 1; Table 2) (Coppe ´ et al., 2010; Kuilman and Peeper, 2009).”
From Cellular Senescence: Defining a Path Forward (2019) · cites this paper as Coppe et al., 2010
The cited source says what the claim attributes to it.
In the citing paper
“For example, the SASP reinforces and spreads senescence in autocrine and paracrine fashions (Acosta et al., 2013; Coppe ´ et al., 2010; Kuilman and Peeper, 2009) and activates immune responses that eliminate senescent cells (Krizhanovsky et al., 2008a; Mun ˜ oz-Espı ´n and Serrano, 2014).”
From Cellular Senescence: Defining a Path Forward (2019) · cites this paper as Coppe et al., 2010
The cited source says what the claim attributes to it.
In the citing paper
“Although cellular senescence can serve as a tumorigenic restrictive mechanism, it can also promote tumor growth and tumor invasiveness, through SASP-mediated regulatory effects”
From Redox control of senescence and age-related disease. (2017) · cites this paper as [105]
The cited source says what the claim attributes to it.
In the citing paper
“Senescent T cells are prevalent among Tem cells, and adopt a pro-inflammatory profile, similarly to the senescence-associated secreting phenotype (SASP) that was observed in fibroblasts [340].”
From Guidelines for the use of flow cytometry and cell sorting in immunological studies (third edition) (2021) · cites this paper as [340]
The cited source says what the claim attributes to it.
In the citing paper
“The SASP can also induce epithelial-to-mesenchymal transition (EMT) and increase tumor vascularization, suggesting that it has mostly protumorigenic properties (Coppé et al. 2010).”
From Senescence and the SASP: many therapeutic avenues (2020) · cites this paper as Coppé et al. 2010
The cited source says what the claim attributes to it.
In the citing paper
“To add extra confusion, the SASP can also differ based on cell type, cause of senescence, or even stage of senescence [37,95].”
From Untangling senescent and damage‐associated microglia in the aging and diseased brain (2023) · cites this paper as [95]
The cited source says what the claim attributes to it.
In the citing paper
“Senescent cells contribute to aging and age-related pathologies21,22,23 through their senescence-associated secretory phenotype (SASP).24,25,26”
From Uncovering the signatures of aging and senescence in the human dorsolateral prefrontal cortex (2026) · cites this paper as [24]
In the citing paper
“recent evidence suggests that senescent cells can morph their phenotype to SASP, which can paradoxically cause tumor growth (Coppé et al. 2010).”
From Benefits of Metformin in Attenuating the Hallmarks of Aging (2020) · cites this paper as Coppé et al. 2010
In the citing paper
“Although senescence acts as a protective mechanism against malignancies, serving as a tumor-suppressive mechanism”
From Benefits of Metformin in Attenuating the Hallmarks of Aging (2020) · cites this paper as Coppé et al. 2010
In the citing paper
“these factors promote shedding of membrane-associated proteins, degradation of signaling molecules, and/or ECM processing, thereby disrupting normal tissue framework and function”
From Redox control of senescence and age-related disease. (2017) · cites this paper as [72]
In the citing paper
“senescent cells display extensive changes in gene expression, including the expression and secretion of many proinflammatory cytokines, chemokines, growth factors, and proteases; collectively these features are termed the senescence-associated secretory phenotype (SASP) (2, 7–10).”
From The DNA damage response induces inflammation and senescence by inhibiting autophagy of GATA4. (2015) · cites this paper as [9]
In the citing paper
“Senescence-associated secretory phenotype (SASP) converts senescent cells into continuous sources of pro-inflammatory mediators, reactive oxygen species and metalloproteinases [43].”
From Ageing, Cellular Senescence and Neurodegenerative Disease (2018) · cites this paper as [43]
In the citing paper
“SASP consists of chemokines, cytokines, growth factors and metaloproteinases [43].”
From Ageing, Cellular Senescence and Neurodegenerative Disease (2018) · cites this paper as [43]
In the citing paper
“The SCI state in older individuals is thought to be caused in part by a complex process called cellular senescence, which is characterized by an arrest of cell proliferation and the development of a multifaceted senescence-associated secretory phenotype (SASP)53.”
From Chronic inflammation in the etiology of disease across the life span (2019) · cites this paper as [53]
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 [105]
In the citing paper
“sen(IR)-fibroblasts had increased expression of Csf1 transcripts (Extended Data Fig. 5e) and other growth factors40, which we confirmed were significantly increased at the protein level by proteomic analysis of the conditioned medium (Extended Data Fig. 5g).”
From Senescent cells promote tissue NAD+ decline during ageing via the activation of CD38+ macrophages (2020) · cites this paper as [40]
In the citing paper
“We found that IP injections of PZ significantly decreased splenic expression of several SC biomarkers40,41, including Cdkn2a (p16), Cdkn1a (p21), and the SASP factors Il6, Cxcl12, Mmp3, and Tnfsf11 (Rankl) mRNA (Fig. 3e–j), indicating that PZ can effectively clear SCs in naturally aged mice.”
From Using proteolysis-targeting chimera technology to reduce navitoclax platelet toxicity and improve its senolytic activity (2020) · cites this paper as [41]
In the citing paper
“Most senescent cells develop altered secretory activities known as a senescence-associated secretory phenotype (SASP) 77,78 .”
From Vascular smooth muscle cells in atherosclerosis (2019) · cites this paper as [77]
In the citing paper
“Furthermore, senescent cells secrete bioactive mediators, including degradative enzymes, inflammatory cytokines and growth factors, which may further drive stem cell dysfunction with aging127.”
From Stem cell aging: mechanisms, regulators and therapeutic opportunities (2014) · cites this paper as [127]
In the citing paper
“Accumulation of senescent cells in aging tissues can be another driver of chronic inflammation, as these cells secrete inflammatory factors, growth regulators, proteases and other signaling molecules127, affecting neighboring cells in the local environment and promoting senescence and inflammation.”
From Stem cell aging: mechanisms, regulators and therapeutic opportunities (2014) · cites this paper as [127]
In the citing paper
“senescent cells actively communicate with neighbouring cells and the extracellular matrix through a plethora of secretory factors, including extracellular proteases, cytokines and chemokines, and growth factors.”
From Inside and out: the activities of senescence in cancer (2014) · cites this paper as [90]
In the citing paper
“Components of the SASP have been shown to act in a paracrine manner, inducing senescence in surrounding cells, and this is thought to be a mechanism by which senescent cells contribute to age-related tissue dysfunction (Acosta et al., 2013; Baker et al., 2016; Coppé et al., 2010; Nelson et al., 2012).”
From Cytoplasmic DNA: sources, sensing, and role in aging and disease (2021) · cites this paper as Coppé et al., 2010
In the citing paper
“An unexpected property of senescent fibroblasts was their ability to secrete a wide array of proinflammatory cytokines including IL-6 and IL-1 and also other biological mediators such as matrix metalloproteinases [41].”
From Senescence of T Lymphocytes: Implications for Enhancing Human Immunity (2016) · cites this paper as [41]
In the citing paper
“This is known as the senescence associated secretory phenotype or SASP and is considered to be important for remodelling of ageing tissues [41, 42].”
From Senescence of T Lymphocytes: Implications for Enhancing Human Immunity (2016) · cites this paper as [41]
In the citing paper
“Other senescence markers previously used with other cell types, including formation of HP1-γ foci (28,29), spontaneous induction of γ-H2AX foci (30), and mRNA expression of SASP factors, such as IL6, IL8, CXCR1, and CXCR2 (8), were also increased in the CD28 -CD57 + subset”
From p53 isoforms regulate aging- and tumor-associated replicative senescence in T lymphocytes (2013) · cites this paper as [8]
In the citing paper
“In particular, an increase in the basal production of proinflammatory cytokines, observed in different cell types, could be a major contributor to the age-related increase of the levels of such molecules observed in several cohorts of elderly subjects [19, 67, 68].”
From Aging of the immune system: Focus on inflammation and vaccination (2016) · cites this paper as [19]
In the citing paper
“Although the SASP is a feature shared by different senescence types, its regulation is considerably heterogeneous and is influenced by the cell type and the level and exposure duration to the initial senescence inducer [149].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [149]
In the citing paper
“Indeed, some types of cellular senescence, including the telomere-induced replicative type, are associated with an in vitro senescence-associated secretory phenotype (SASP), where cytokines and proteases are detected in culture media120.”
From The telomere syndromes (2012) · cites this paper as [120]
In the citing paper
“In addition, senescent cells express the cell cycle inhibitor p16INK4A (p16), senescence-associated β-galatosidase (SA-βgal), and an altered expression profile known as the senescence-associated secretory phenotype (SASP)11.”
From Stromal senescence establishes an immunosuppressive microenvironment that drives tumorigenesis (2016) · cites this paper as [11]
In the citing paper
“p27-induced senescence, which induces a SASP reminiscent of that observed in fibroblasts undergoing chronologic aging11.”
From Stromal senescence establishes an immunosuppressive microenvironment that drives tumorigenesis (2016) · cites this paper as [11]
In the citing paper
“The mechanisms responsible for the paradoxical role that senescence plays in tumorigenesis have remained obscure but are likely to lie in the senescent secretory profile that is defined by the cell of origin11.”
From Stromal senescence establishes an immunosuppressive microenvironment that drives tumorigenesis (2016) · cites this paper as [11]
In the citing paper
“On the other hand, the SASP can create a pro-tumorigenic environment (Coppe et al., 2010; Krtolica et al., 2001; Ruhland et al., 2016).”
From CDK4/6 Inhibitors: The Mechanism of Action May Not Be as Simple as Once Thought (2018) · cites this paper as Coppe et al., 2010
In the citing paper
“Metformin has also been reported to offset the effects of aging in the elderly and in cardiovascular disease (194, 198–200).”
From A Critical Review of the Evidence That Metformin Is a Putative Anti-Aging Drug That Enhances Healthspan and Extends Lifespan (2021) · cites this paper as [194]
In the citing paper
“Several other studies using a variety of different cell types have reported that metformin inhibits NF-κB activation, decreases the production of inflammatory cytokines and the genes that code for the inflammatory response thus supporting the healthspan benefits of metformin (105, 194–196).”
From A Critical Review of the Evidence That Metformin Is a Putative Anti-Aging Drug That Enhances Healthspan and Extends Lifespan (2021) · cites this paper as [194]
In the citing paper
“Senescent cells secrete a range of interleukins, inflammatory cytokines and growth factors (collectively referred to as SASP) that can affect surrounding cells (35).”
From Senolytic Combination of Dasatinib and Quercetin Alleviates Intestinal Senescence and Inflammation and Modulates the Gut Microbiome in Aged Mice (2021) · cites this paper as [35]
In the citing paper
“They have a distinctive phenotype, characterized by profound chromatin alterations and the development of a senescence-associated secretory phenotype (SASP), mainly comprised of cytokines, chemokines, matrix remodeling proteins, and growth factors, that has deleterious effects on tissue function, both locally and systemically”
From Skeletal muscle aging, cellular senescence, and senotherapeutics: current knowledge and future directions (2021) · cites this paper as Coppé et al., 2010
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 [5]
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 [5]
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 [5]
In the citing paper
“Cells present in the tumour microenvironment, such as fibroblasts, can become senescent and promote the growth and proliferation of tumour cells.7,39,40”
From Paracrine roles of cellular senescence in promoting tumourigenesis (2018) · cites this paper as [7]
In the citing paper
“There is mounting evidence that dysregulation or inappropriate activation of senescence contributes to tumour progression and malignancy.5,7,17”
From Paracrine roles of cellular senescence in promoting tumourigenesis (2018) · cites this paper as [7]
In the citing paper
“Senescent cells can contribute to the acquisition of invasive and metastatic properties of cancer cells, as well as the induction of tumour-associated angiogenesis.7,39”
From Paracrine roles of cellular senescence in promoting tumourigenesis (2018) · cites this paper as [7]
In the citing paper
“In this regard, the SASP has been shown to promote inflammation.7,72”
From Paracrine roles of cellular senescence in promoting tumourigenesis (2018) · cites this paper as [7]
In the citing paper
“telomere attrition accompanying each round of proliferation, leading to arrested cell division or ‘replicative senescence’”
From Evolution of the immune system in humans from infancy to old age (2015) · cites this paper as [99]
In the citing paper
“A third more recent addition to these fundamental changes of aged cells is the acquisition of the SASP, contributing to increased pro-inflammatory cytokine secretion and low-grade inflammation [99].”
From Evolution of the immune system in humans from infancy to old age (2015) · cites this paper as [99]
In the citing paper
“In elderly patients, a systemic abundance of proinflammatory cytokines (IL-1, TNF, and IL-6) can be detected, which is called senescence-associated secretory phenotype (SASP).45”
From Inflammatory bone marrow microenvironment (2019) · cites this paper as [45]
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Citations
Cites
Coussens, L. M., & Werb, Z. (2002) · Nature · doi:10.1038/nature01322 · Cited by 15,111
Oxidants, oxidative stress and the biology of ageing
Finkel, T., & Holbrook, N. J. (2000) · Nature · doi:10.1038/35041687 · Cited by 9,413
A biomarker that identifies senescent human cells in culture and in aging skin in vivo.
Dimri, G. P., Lee, X., Basile, G., Acosta, M., Scott, G., Roskelley, C., Medrano, E. E., Linskens, M., Rubelj, I., & Pereira-Smith, O. (1995) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.92.20.9363 · Cited by 7,477
Epithelial–mesenchymal transitions in tumour progression
Thiery, J. P. (2002) · Nature reviews. Cancer · doi:10.1038/nrc822 · Cited by 6,767
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
Self-citationMitochondria, Oxidants, and Aging
Balaban, R. S., Nemoto, S., & Finkel, T. (2005) · Cell · doi:10.1016/j.cell.2005.02.001 · Cited by 4,388
Met, metastasis, motility and more
Birchmeier, C., Birchmeier, W., Gherardi, E., & Woude, G. F. V. (2003) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm1261 · Cited by 2,652
Senescence and tumour clearance is triggered by p53 restoration in murine liver carcinomas
Xue, W., Zender, L., Miething, C., Dickins, R. A., Hernando, E., Krizhanovsky, V., Cordon-Cardo, C., & Lowe, S. W. (2007) · Nature · doi:10.1038/nature05529 · Cited by 2,473
Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors
Campisi, J. (2005) · Cell · doi:10.1016/j.cell.2005.02.003 · Cited by 2,379
Self-citationCancer and the chemokine network
Balkwill, F. (2004) · Nature Reviews Cancer · doi:10.1038/nrc1388 · Cited by 2,343
Research works printed but not linked: 5
- Untergasser G, 2002, Cancer Res., 62, 6255
- Barcellos-Hoff MH, 2000, Cancer Res., 60, 1254
- Balentien E, 1991, Oncogene, 6, 1115
- Camphausen K, 2001, Cancer Res., 61, 2207
- Qian LW, 2002, Clin. Cancer Res., 8, 1223
Cited by
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Chronic inflammation in the etiology of disease across the life span
Furman, D., Campisi, J., Verdin, E., Carrera-Bastos, P., Targ, S., Franceschi, C., Ferrucci, L., Gilroy, D. W., Fasano, A., Miller, G. W., et al. (2019) · Nature Medicine · doi:10.1038/s41591-019-0675-0 · Cited by 4,915
Self-citationThe extracellular matrix at a glance
Frantz, C., Stewart, K. M., & Weaver, V. M. (2010) · Journal of Cell Science · doi:10.1242/jcs.023820 · Cited by 4,334
Chronic Inflammation (Inflammaging) and Its Potential Contribution to Age-Associated Diseases
Franceschi, C., & Campisi, J. (2014) · The Journals of Gerontology Series A: Biological Sciences and Medical Sciences · doi:10.1093/gerona/glu057 · Cited by 3,891
Self-citationCellular Senescence: Defining a Path Forward
Gorgoulis, V., Adams, P. D., Alimonti, A., Bennett, D. C., Bischof, O., Bishop, C., Campisi, J., Collado, M., Evangelou, K., Ferbeyre, G., et al. (2019) · Cell · doi:10.1016/j.cell.2019.10.005 · Cited by 3,225
Self-citationAgeing as a risk factor for neurodegenerative disease
Hou, Y., Dan, X., Babbar, M., Wei, Y., Hasselbalch, S. G., Croteau, D. L., & Bohr, V. A. (2019) · Nature Reviews Neurology · doi:10.1038/s41582-019-0244-7 · Cited by 3,310
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
Hallmarks of Cellular Senescence
Hernandez-Segura, A., Nehme, J., & Demaria, M. (2018) · Trends in Cell Biology · doi:10.1016/j.tcb.2018.02.001 · Cited by 2,605
Distinct populations of inflammatory fibroblasts and myofibroblasts in pancreatic cancer
Öhlund, D., Handly-Santana, A., Biffi, G., Elyada, E., Almeida, A. S., Ponz-Sarvise, M., Corbo, V., Oni, T. E., Hearn, S. A., Lee, E. J., et al. (2017) · Journal of Experimental Medicine · doi:10.1084/jem.20162024 · Cited by 2,590
The role of senescent cells in ageing
van Deursen, J. M. (2014) · Nature · doi:10.1038/nature13193 · Cited by 2,623
Cellular senescence in aging and age-related disease: from mechanisms to therapy
Childs, B. G., Durik, M., Baker, D. J., & van Deursen, J. M. (2015) · Nature Medicine · doi:10.1038/nm.4000 · Cited by 2,363
Cellular senescence in ageing: from mechanisms to therapeutic opportunities
Di Micco, R., Krizhanovsky, V., Baker, D., & d’Adda di Fagagna, F. (2021) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-020-00314-w · Cited by 2,277
An Essential Role for Senescent Cells in Optimal Wound Healing through Secretion of PDGF-AA
Demaria, M., Ohtani, N., Youssef, S. A., Rodier, F., Toussaint, W., Mitchell, J. R., Laberge, R.-M., Vijg, J., Van Steeg, H., Dollé, M. E. T., et al. (2014) · Developmental Cell · doi:10.1016/j.devcel.2014.11.012 · Cited by 2,045
“Senescent cells most likely promote aging through their senescence-associated secretory phenotype (SASP): the increased expression and secretion of a suite of inflammatory cytokines, chemokines, growth factors, and proteases (Coppé et al., 2010a; van Deursen, 2014).”
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Kawai, T., Autieri, M. V., & Scalia, R. (2021) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00379.2020 · Cited by 1,947
Clearance of senescent cells by ABT263 rejuvenates aged hematopoietic stem cells in mice
Chang, J., Wang, Y., Shao, L., Laberge, R.-M., Demaria, M., Campisi, J., Janakiraman, K., Sharpless, N. E., Ding, S., Feng, W., et al. (2016) · Nature Medicine · doi:10.1038/nm.4010 · Cited by 1,819
Self-citationEvolution of the immune system in humans from infancy to old age
Simon, A. K., Hollander, G. A., & McMichael, A. (2015) · Proceedings of the Royal Society B: Biological Sciences · doi:10.1098/rspb.2014.3085 · Cited by 1,796
Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype
Kumari, R., & Jat, P. (2021) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2021.645593 · Cited by 1,622
CDK4/6 inhibition triggers anti-tumour immunity
Goel, S., DeCristo, M. J., Watt, A. C., BrinJones, H., Sceneay, J., Li, B. B., Khan, N., Ubellacker, J. M., Xie, S., Metzger-Filho, O., et al. (2017) · Nature · doi:10.1038/nature23465 · Cited by 1,513
A proteomic atlas of senescence-associated secretomes for aging biomarker development
Basisty, N., Kale, A., Jeon, O. H., Kuehnemann, C., Payne, T., Rao, C., Holtz, A., Shah, S., Sharma, V., Ferrucci, L., et al. (2020) · PLOS Biology · doi:10.1371/journal.pbio.3000599 · Cited by 1,348
Self-citationInflammatory networks during cellular senescence: causes and consequences.
Freund, A., Orjalo, A. V., Desprez, P.-Y., & Campisi, J. (2010) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2010.03.003 · Cited by 1,354
Self-citationThe cGAS–cGAMP–STING pathway connects DNA damage to inflammation, senescence, and cancer
Li, T., & Chen, Z. J. (2018) · Journal of Experimental Medicine · doi:10.1084/jem.20180139 · Cited by 1,293
Diversity and biology of cancer-associated fibroblasts
Biffi, G., & Tuveson, D. A. (2021) · Physiological Reviews · doi:10.1152/physrev.00048.2019 · Cited by 1,265
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
L1 drives IFN in senescent cells and promotes age-associated inflammation
De Cecco, M., Ito, T., Petrashen, A. P., Elias, A. E., Skvir, N. J., Criscione, S. W., Caligiana, A., Brocculi, G., Adney, E. M., Boeke, J. D., et al. (2019) · Nature · doi:10.1038/s41586-018-0784-9 · Cited by 1,255
“Observed: qPCR was performed on 1 ng of genomic DNA and normalized to a known single copy locus. i , Activation of IFN-α and IFN-β 1 genes during senescence of WI-38 and IMR-90 cells was determined by RT-qPCR. j, Confirmation of the senescent status of cells in OIS (20 days, Fig.”
InfluentialAge 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
Senescence and aging: Causes, consequences, and therapeutic avenues
McHugh, D., & Gil, J. (2018) · Journal of Cell Biology · doi:10.1083/jcb.201708092 · Cited by 1,233
Senolytics in idiopathic pulmonary fibrosis: Results from a first-in-human, open-label, pilot study
Justice, J. N., Nambiar, A. M., Tchkonia, T., LeBrasseur, N. K., Pascual, R., Hashmi, S. K., Prata, L., Masternak, M. M., Kritchevsky, S. B., Musi, N., et al. (2019) · EBioMedicine · doi:10.1016/j.ebiom.2018.12.052 · Cited by 1,261
Mechanisms and functions of cellular senescence
Herranz, N., & Gil, J. (2018) · Journal of Clinical Investigation · doi:10.1172/jci95148 · Cited by 1,232
Innate immune sensing of cytosolic chromatin fragments through cGAS promotes senescence
Glück, S., Guey, B., Gulen, M. F., Wolter, K., Kang, T.-W., Schmacke, N. A., Bridgeman, A., Rehwinkel, J., Zender, L., & Ablasser, A. (2017) · Nature Cell Biology · doi:10.1038/ncb3586 · Cited by 1,196
“Cyclic [G(2,5)pA(3,5)p] is the metazoan second messenger produced by DNA-activated cyclic GMP-AMP synthase.”
Targeting cellular senescence prevents age-related bone loss in mice
Farr, J. N., Xu, M., Weivoda, M. M., Monroe, D. G., Fraser, D. G., Onken, J. L., Negley, B. A., Sfeir, J. G., Ogrodnik, M. B., Hachfeld, C. M., et al. (2017) · Nature Medicine · doi:10.1038/nm.4385 · Cited by 1,182
Senescence is a developmental mechanism that contributes to embryonic growth and patterning
Storer, M., Mas, A., Robert-Moreno, A., Pecoraro, M., Ortells, M. C., Di Giacomo, V., Yosef, R., Pilpel, N., Krizhanovsky, V., Sharpe, J., et al. (2013) · Cell · doi:10.1016/j.cell.2013.10.041 · Cited by 1,186
Senescence and the SASP: many therapeutic avenues
Birch, J., & Gil, J. (2020) · Genes & Development · doi:10.1101/gad.343129.120 · Cited by 1,177
“The SASP can also induce epithelial-to-mesenchymal transition (EMT) and increase tumor vascularization, suggesting that it has mostly protumorigenic properties (Coppé et al. 2010).”
BackgroundSenescence-associated reprogramming promotes cancer stemness
Milanovic, M., Fan, D. N. Y., Belenki, D., Däbritz, J. H. M., Zhao, Z., Yu, Y., Dörr, J. R., Dimitrova, L., Lenze, D., Monteiro Barbosa, I. A., et al. (2018) · Nature · doi:10.1038/nature25167 · Cited by 1,131
Laberge, R.-M., Sun, Y., Orjalo, A. V., Patil, C. K., Freund, A., Zhou, L., Curran, S. C., Davalos, A. R., Wilson-Edell, K. A., Liu, S., et al. (2015) · Nature Cell Biology · doi:10.1038/ncb3195 · Cited by 1,160
Self-citationCellular senescence and senolytics: the path to the clinic
Chaib, S., Tchkonia, T., & Kirkland, J. L. (2022) · Nature Medicine · doi:10.1038/s41591-022-01923-y · Cited by 1,134
ROS, Cell Senescence, and Novel Molecular Mechanisms in Aging and Age‐Related Diseases
Davalli, P., Mitic, T., Caporali, A., Lauriola, A., & D’Arca, D. (2016) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2016/3565127 · Cited by 1,059
Freund, A., Patil, C. K., & Campisi, J. (2011) · The EMBO Journal · doi:10.1038/emboj.2011.69 · Cited by 1,039
Self-citationAge-dependent dysregulation of innate immunity
Shaw, A. C., Goldstein, D. R., & Montgomery, R. R. (2013) · Nature Reviews Immunology · doi:10.1038/nri3547 · Cited by 1,061
Mitochondrial dysfunction in cell senescence and aging
Miwa, S., Kashyap, S., Chini, E., & von Zglinicki, T. (2022) · Journal of Clinical Investigation · doi:10.1172/jci158447 · Cited by 1,061
A new gene set identifies senescent cells and predicts senescence-associated pathways across tissues
Saul, D., Kosinsky, R. L., Atkinson, E. J., Doolittle, M. L., Zhang, X., LeBrasseur, N. K., Pignolo, R. J., Robbins, P. D., Niedernhofer, L. J., Ikeno, Y., et al. (2022) · Nature Communications · doi:10.1038/s41467-022-32552-1 · Cited by 1,022
Fisetin is a senotherapeutic that extends health and lifespan
Yousefzadeh, M. J., Zhu, Y., McGowan, S. J., Angelini, L., Fuhrmann-Stroissnigg, H., Xu, M., Ling, Y. Y., Melos, K. I., Pirtskhalava, T., Inman, C. L., et al. (2018) · EBioMedicine · doi:10.1016/j.ebiom.2018.09.015 · Cited by 1,032
cGAS is essential for cellular senescence
Yang, H., Wang, H., Ren, J., Chen, Q., & Chen, Z. J. (2017) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1705499114 · Cited by 1,009
An aged immune system drives senescence and ageing of solid organs
Yousefzadeh, M. J., Flores, R. R., Zhu, Y., Schmiechen, Z. C., Brooks, R. W., Trussoni, C. E., Cui, Y., Angelini, L., Lee, K.-A., McGowan, S. J., et al. (2021) · Nature · doi:10.1038/s41586-021-03547-7 · Cited by 972
Geriatric muscle stem cells switch reversible quiescence into senescence
Sousa-Victor, P., Gutarra, S., García-Prat, L., Rodriguez-Ubreva, J., Ortet, L., Ruiz-Bonilla, V., Jardí, M., Ballestar, E., González, S., Serrano, A. L., et al. (2014) · Nature · doi:10.1038/nature13013 · Cited by 1,010
Cancer stem cells—Origins and biomarkers: Perspectives for targeted personalized therapies
Walcher, L., Kistenmacher, A.-K., Suo, H., Kitte, R., Dluczek, S., Strauß, A., Blaudszun, A.-R., Yevsa, T., Fricke, S., & Kossatz-Boehlert, U. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.01280 · Cited by 1,007
The Continuum of Aging and Age-Related Diseases: Common Mechanisms but Different Rates
Franceschi, C., Garagnani, P., Morsiani, C., Conte, M., Santoro, A., Grignolio, A., Monti, D., Capri, M., & Salvioli, S. (2018) · Frontiers in Medicine · doi:10.3389/fmed.2018.00061 · Cited by 945
Armanios, M., & Blackburn, E. H. (2012) · Nature Reviews Genetics · doi:10.1038/nrg3246 · Cited by 982
The DNA damage response induces inflammation and senescence by inhibiting autophagy of GATA4.
Kang, C., Xu, Q., Martin, T. D., Li, M. Z., Demaria, M., Aron, L., Lu, T., Yankner, B. A., Campisi, J., & Elledge, S. J. (2015) · Science · doi:10.1126/science.aaa5612 · Cited by 982
Self-citationTargeting the progression of chronic kidney disease
Ruiz-Ortega, M., Rayego-Mateos, S., Lamas, S., Ortiz, A., & Rodrigues-Diez, R. R. (2020) · Nature Reviews Nephrology · doi:10.1038/s41581-019-0248-y · Cited by 979
Xu, M., Tchkonia, T., Ding, H., Ogrodnik, M., Lubbers, E. R., Pirtskhalava, T., White, T. A., Johnson, K. O., Stout, M. B., Mezera, V., et al. (2015) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1515386112 · Cited by 915
Exploiting 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
How the ageing microenvironment influences tumour progression
Fane, M., & Weeraratna, A. T. (2020) · Nature Reviews Cancer · doi:10.1038/s41568-019-0222-9 · Cited by 849
Brandhorst, S., Choi, I. Y., Wei, M., Cheng, C. W., Sedrakyan, S., Navarrete, G., Dubeau, L., Yap, L. P., Park, R., Vinciguerra, M., et al. (2015) · Cell Metabolism · doi:10.1016/j.cmet.2015.05.012 · Cited by 850
Cellular senescence and its effector programs
Salama, R., Sadaie, M., Hoare, M., & Narita, M. (2014) · Genes & Development · doi:10.1101/gad.235184.113 · Cited by 855
Stem cell aging: mechanisms, regulators and therapeutic opportunities
Oh, J., Lee, Y. D., & Wagers, A. J. (2014) · Nature Medicine · doi:10.1038/nm.3651 · Cited by 796
Measuring biological aging in humans: a quest
Ferrucci, L., Gonzalez‐Freire, M., Fabbri, E., Simonsick, E., Tanaka, T., Moore, Z., Salimi, S., Sierra, F., & de Cabo, R. (2020) · Aging Cell · doi:10.1111/acel.13080 · Cited by 781
Mechanisms and therapeutic implications of cellular senescence in osteoarthritis
Coryell, P. R., Diekman, B. O., & Loeser, R. F. (2021) · Nature Reviews Rheumatology · doi:10.1038/s41584-020-00533-7 · Cited by 761
TGF-β1 Signaling and Tissue Fibrosis
Kim, K. K., Sheppard, D., & Chapman, H. A. (2018) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a022293 · Cited by 800
Causes, consequences, and reversal of immune system aging
Montecino-Rodriguez, E., Berent-Maoz, B., & Dorshkind, K. (2013) · Journal of Clinical Investigation · doi:10.1172/jci64096 · Cited by 793
mTOR regulates MAPKAPK2 translation to control the senescence-associated secretory phenotype
Herranz, N., Gallage, S., Mellone, M., Wuestefeld, T., Klotz, S., Hanley, C. J., Raguz, S., Acosta, J. C., Innes, A. J., Banito, A., et al. (2015) · Nature Cell Biology · doi:10.1038/ncb3225 · Cited by 788
Salminen, A., Kauppinen, A., & Kaarniranta, K. (2012) · Cellular Signalling · doi:10.1016/j.cellsig.2011.12.006 · Cited by 763
Benefits of Metformin in Attenuating the Hallmarks of Aging
Kulkarni, A. S., Gubbi, S., & Barzilai, N. (2020) · Cell Metabolism · doi:10.1016/j.cmet.2020.04.001 · Cited by 766
Kerur, N., Veettil, M. V., Sharma-Walia, N., Bottero, V., Sadagopan, S., Otageri, P., & Chandran, B. (2011) · Cell Host & Microbe · doi:10.1016/j.chom.2011.04.008 · Cited by 702
Moiseeva, O., Deschênes‐Simard, X., St‐Germain, E., Igelmann, S., Huot, G., Cadar, A. E., Bourdeau, V., Pollak, M. N., & Ferbeyre, G. (2013) · Aging Cell · doi:10.1111/acel.12075 · Cited by 654
A guide to assessing cellular senescence in vitro and in vivo
González‐Gualda, E., Baker, A. G., Fruk, L., & Muñoz‐Espín, D. (2021) · The FEBS Journal · doi:10.1111/febs.15570 · Cited by 645
Telomeres: history, health, and hallmarks of aging
Chakravarti, D., LaBella, K. A., & DePinho, R. A. (2021) · Cell · doi:10.1016/j.cell.2020.12.028 · Cited by 637
Role of p53 in the Regulation of Cellular Senescence
Mijit, M., Caracciolo, V., Melillo, A., Amicarelli, F., & Giordano, A. (2020) · Biomolecules · doi:10.3390/biom10030420 · Cited by 639
Senescent cells as a source of inflammatory factors for tumor progression
Davalos, A. R., Coppe, J.-P., Campisi, J., & Desprez, P.-Y. (2010) · Cancer and Metastasis Reviews · doi:10.1007/s10555-010-9220-9 · Cited by 636
Self-citationCellular senescence: a key therapeutic target in aging and diseases
Zhang, L., Pitcher, L. E., Yousefzadeh, M. J., Niedernhofer, L. J., Robbins, P. D., & Zhu, Y. (2022) · Journal of Clinical Investigation · doi:10.1172/jci158450 · Cited by 631
Sleep health: Reciprocal regulation of sleep and innate immunity
Irwin, M. R., & Opp, M. R. (2017) · Neuropsychopharmacology · doi:10.1038/npp.2016.148 · Cited by 624
Interventions to slow aging in humans: are we ready?
Longo, V. D., Antebi, A., Bartke, A., Barzilai, N., Brown‐Borg, H. M., Caruso, C., Curiel, T. J., Cabo, R., Franceschi, C., Gems, D., et al. (2015) · Aging Cell · doi:10.1111/acel.12338 · Cited by 592
“Cellular senescence is associated with a pro-inflammatory senescence-associated secretory phenotype (SASP), which is triggered by damaging agents (radiation, viruses) and possibly by continuous exposure to cellular debris (Coppe et al., 2010).”
The dynamic nature of senescence in cancer
Lee, S., & Schmitt, C. A. (2019) · Nature Cell Biology · doi:10.1038/s41556-018-0249-2 · Cited by 588
Eggert, T., Wolter, K., Ji, J., Ma, C., Yevsa, T., Klotz, S., Medina-Echeverz, J., Longerich, T., Forgues, M., Reisinger, F., et al. (2016) · Cancer Cell · doi:10.1016/j.ccell.2016.09.003 · Cited by 609
Astrocyte Senescence as a Component of Alzheimer’s Disease
Bhat, R., Crowe, E. P., Bitto, A., Moh, M., Katsetos, C. D., Garcia, F. U., Johnson, F. B., Trojanowski, J. Q., Sell, C., & Torres, C. (2012) · PLoS ONE · doi:10.1371/journal.pone.0045069 · Cited by 586
Plasma proteomic signature of age in healthy humans
Tanaka, T., Biancotto, A., Moaddel, R., Moore, A. Z., Gonzalez‐Freire, M., Aon, M. A., Candia, J., Zhang, P., Cheung, F., Fantoni, G., et al. (2018) · Aging Cell · doi:10.1111/acel.12799 · Cited by 562
Frailty and sarcopenia: The potential role of an aged immune system
Wilson, D., Jackson, T., Sapey, E., & Lord, J. M. (2017) · Ageing Research Reviews · doi:10.1016/j.arr.2017.01.006 · Cited by 573
Impaired immune surveillance accelerates accumulation of senescent cells and aging
Ovadya, Y., Landsberger, T., Leins, H., Vadai, E., Gal, H., Biran, A., Yosef, R., Sagiv, A., Agrawal, A., Shapira, A., et al. (2018) · Nature Communications · doi:10.1038/s41467-018-07825-3 · Cited by 578
Spatial Coupling of mTOR and Autophagy Augments Secretory Phenotypes
Narita, M., Young, A. R. J., Arakawa, S., Samarajiwa, S. A., Nakashima, T., Yoshida, S., Hong, S., Berry, L. S., Reichelt, S., Ferreira, M., et al. (2011) · Science · doi:10.1126/science.1205407 · Cited by 594
Identification of senescent cells in the bone microenvironment
Farr, J. N., Fraser, D. G., Wang, H., Jaehn, K., Ogrodnik, M. B., Weivoda, M. M., Drake, M. T., Tchkonia, T., LeBrasseur, N. K., Kirkland, J. L., et al. (2016) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.2892 · Cited by 562
Measuring biological age using omics data
Rutledge, J., Oh, H., & Wyss-Coray, T. (2022) · Nature Reviews Genetics · doi:10.1038/s41576-022-00511-7 · Cited by 570
Senescent cells evade immune clearance via HLA-E-mediated NK and CD8+ T cell inhibition
Pereira, B. I., Devine, O. P., Vukmanovic-Stejic, M., Chambers, E. S., Subramanian, P., Patel, N., Virasami, A., Sebire, N. J., Kinsler, V., Valdovinos, A., et al. (2019) · Nature Communications · doi:10.1038/s41467-019-10335-5 · Cited by 556
Self-citationThe role of cellular senescence in ageing and endocrine disease
Khosla, S., Farr, J. N., Tchkonia, T., & Kirkland, J. L. (2020) · Nature Reviews Endocrinology · doi:10.1038/s41574-020-0335-y · Cited by 523
Cellular and molecular biology of aging endothelial cells
Donato, A. J., Morgan, R. G., Walker, A. E., & Lesniewski, L. A. (2015) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2015.01.021 · Cited by 538
Mechanisms underlying T cell ageing
Goronzy, J. J., & Weyand, C. M. (2019) · Nature Reviews Immunology · doi:10.1038/s41577-019-0180-1 · Cited by 506
Guidelines for the use of flow cytometry and cell sorting in immunological studies (third edition)
Cossarizza, A., Chang, H., Radbruch, A., Abrignani, S., Addo, R., Akdis, M., Andrä, I., Andreata, F., Annunziato, F., Arranz, E., et al. (2021) · European Journal of Immunology · doi:10.1002/eji.202170126 · Cited by 531
Coppé, J.-P., Rodier, F., Patil, C. K., Freund, A., Desprez, P.-Y., & Campisi, J. (2011) · Journal of Biological Chemistry · doi:10.1074/jbc.m111.257071 · Cited by 506
Self-citationStrategies for targeting senescent cells in human disease
Gasek, N. S., Kuchel, G. A., Kirkland, J. L., & Xu, M. (2021) · Nature Aging · doi:10.1038/s43587-021-00121-8 · Cited by 501
Senescent cell clearance by the immune system: Emerging therapeutic opportunities
Prata, L. G. P. L., Ovsyannikova, I. G., Tchkonia, T., & Kirkland, J. L. (2018) · Seminars in Immunology · doi:10.1016/j.smim.2019.04.003 · Cited by 497
Stromal senescence establishes an immunosuppressive microenvironment that drives tumorigenesis
Ruhland, M. K., Loza, A. J., Capietto, A.-H., Luo, X., Knolhoff, B. L., Flanagan, K. C., Belt, B. A., Alspach, E., Leahy, K., Luo, J., et al. (2016) · Nature Communications · doi:10.1038/ncomms11762 · Cited by 496
Pan-cancer single-cell RNA-seq identifies recurring programs of cellular heterogeneity
Kinker, G. S., Greenwald, A. C., Tal, R., Orlova, Z., Cuoco, M. S., McFarland, J. M., Warren, A., Rodman, C., Roth, J. A., Bender, S. A., et al. (2020) · Nature Genetics · doi:10.1038/s41588-020-00726-6 · Cited by 445
Kurppa, K. J., Liu, Y., To, C., Zhang, T., Fan, M., Vajdi, A., Knelson, E. H., Xie, Y., Lim, K., Cejas, P., et al. (2020) · Cancer Cell · doi:10.1016/j.ccell.2019.12.006 · Cited by 475
Acceleration of β Cell Aging Determines Diabetes and Senolysis Improves Disease Outcomes
Aguayo-Mazzucato, C., Andle, J., Lee, T. B., Midha, A., Talemal, L., Chipashvili, V., Hollister-Lock, J., van Deursen, J., Weir, G., & Bonner-Weir, S. (2019) · Cell Metabolism · doi:10.1016/j.cmet.2019.05.006 · Cited by 469
Schaer, D. A., Beckmann, R. P., Dempsey, J. A., Huber, L., Forest, A., Amaladas, N., Li, Y., Wang, Y. C., Rasmussen, E. R., Chin, D., et al. (2018) · Cell Reports · doi:10.1016/j.celrep.2018.02.053 · Cited by 469
Inside and out: the activities of senescence in cancer
Pérez-Mancera, P. A., Young, A. R. J., & Narita, M. (2014) · Nature Reviews Cancer · doi:10.1038/nrc3773 · Cited by 462
Ageing, Cellular Senescence and Neurodegenerative Disease
Kritsilis, M., V. Rizou, S., Koutsoudaki, P. N., Evangelou, K., Gorgoulis, V. G., & Papadopoulos, D. (2018) · International Journal of Molecular Sciences · doi:10.3390/ijms19102937 · Cited by 448
CHK2 kinase in the DNA damage response and beyond
Zannini, L., Delia, D., & Buscemi, G. (2014) · Journal of Molecular Cell Biology · doi:10.1093/jmcb/mju045 · Cited by 455
Novais, E. J., Tran, V. A., Johnston, S. N., Darris, K. R., Roupas, A. J., Sessions, G. A., Shapiro, I. M., Diekman, B. O., & Risbud, M. V. (2021) · Nature Communications · doi:10.1038/s41467-021-25453-2 · Cited by 440
p53-dependent release of Alarmin HMGB1 is a central mediator of senescent phenotypes
Davalos, A. R., Kawahara, M., Malhotra, G. K., Schaum, N., Huang, J., Ved, U., Beausejour, C. M., Coppe, J.-P., Rodier, F., & Campisi, J. (2013) · Journal of Cell Biology · doi:10.1083/jcb.201206006 · Cited by 439
Self-citationCoppé, J.-P., Patil, C. K., Rodier, F., Krtolica, A., Beauséjour, C. M., Parrinello, S., Hodgson, J. G., Chin, K., Desprez, P.-Y., & Campisi, J. (2010) · PLoS ONE · doi:10.1371/journal.pone.0009188 · Cited by 455
Self-citation
Metadata
- Authors
- Coppé, J.-P., Desprez, P.-Y., Krtolica, A., & Campisi, J.
- Affiliations
- Lawrence Berkeley National Laboratory (US)
- Buck Institute for Research on Aging (US)
- Venue
- Annual Review of Pathology: Mechanisms of Disease
- Publisher
- Annual Reviews
- Published
- 2010-01-01
- Volume
- 5
- Issue
- 1
- Pages
- 99-118
- ISSN
- 1553-4006 (ISSN-L)
- 1553-4014
- PMC
- PMC4166495
- OpenAlex
- W2115852450
- Cited by
- 5,206
- References
- 150
- Citations by year
- 2026: 512 · 2025: 540 · 2024: 558 · 2023: 555 · 2022: 560 · 2021: 512 · 2020: 451 · 2019: 317 · 2018: 293 · 2017: 220 · 2016: 178 · 2015: 151 · 2014: 120 · 2013: 87 · 2012: 69
- FWCI
- 7.76
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Annual Review of Pathology Mechanisms of Disease (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (R37AG009909, P01AG041122, P01AG017242)
- 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
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Keywords
- senescence-associated secretory phenotype, cellular senescence, tumor suppression, senescent fibroblasts, tumor microenvironment, inflammation, tumor progression, malignant transformation
- MeSH terms
- Cell Transformation, Neoplastic, Fibroblasts, Humans, Neoplasms, Phenotype, Cellular Senescence, Tumor Suppressor Proteins
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