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The Senescence-Associated Secretory Phenotype: The Dark Side of Tumor Suppression
Open accessAbstract
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 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
“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
“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
“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]
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
“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]
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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Maus, M., López-Polo, V., Mateo, L., Lafarga, M., Aguilera, M., De Lama, E., Meyer, K., Sola, A., Lopez-Martinez, C., López-Alonso, I., et al. (2023) · Nature Metabolism · doi:10.1038/s42255-023-00928-2 · Cited by 215
Fletcher-Sananikone, E., Kanji, S., Tomimatsu, N., Di Cristofaro, L. F. M., Kollipara, R. K., Saha, D., Floyd, J. R., Sung, P., Hromas, R., Burns, T. C., et al. (2021) · Cancer Research · doi:10.1158/0008-5472.can-21-0752 · Cited by 212
Small Extracellular Vesicles Have GST Activity and Ameliorate Senescence-Related Tissue Damage
Fafián-Labora, J. A., Rodríguez-Navarro, J. A., & O’Loghlen, A. (2020) · Cell Metabolism · doi:10.1016/j.cmet.2020.06.004 · Cited by 203
Characterization of cellular senescence in aging skeletal muscle
Zhang, X., Habiballa, L., Aversa, Z., Ng, Y. E., Sakamoto, A. E., Englund, D. A., Pearsall, V. M., White, T. A., Robinson, M. M., Rivas, D. A., et al. (2022) · Nature Aging · doi:10.1038/s43587-022-00250-8 · Cited by 206
Mechanisms of Selective Autophagy in Normal Physiology and Cancer
Mancias, J. D., & Kimmelman, A. C. (2016) · Journal of Molecular Biology · doi:10.1016/j.jmb.2016.02.027 · Cited by 196
Immunosurveillance of senescent cells: the bright side of the senescence program
Sagiv, A., & Krizhanovsky, V. (2013) · Biogerontology · doi:10.1007/s10522-013-9473-0 · Cited by 208
Herdy, J. R., Traxler, L., Agarwal, R. K., Karbacher, L., Schlachetzki, J. C. M., Boehnke, L., Zangwill, D., Galasko, D., Glass, C. K., Mertens, J., et al. (2022) · Cell Stem Cell · doi:10.1016/j.stem.2022.11.010 · Cited by 208
The Cancer SENESCopedia: A delineation of cancer cell senescence
Jochems, F., Thijssen, B., De Conti, G., Jansen, R., Pogacar, Z., Groot, K., Wang, L., Schepers, A., Wang, C., Jin, H., et al. (2021) · Cell Reports · doi:10.1016/j.celrep.2021.109441 · Cited by 201
SASP mediates chemoresistance and tumor-initiating-activity of mesothelioma cells
Canino, C., Mori, F., Cambria, A., Diamantini, A., Germoni, S., Alessandrini, G., Borsellino, G., Galati, R., Battistini, L., Blandino, R., et al. (2012) · Oncogene · doi:10.1038/onc.2011.485 · Cited by 200
Generation of a p16 Reporter Mouse and Its Use to Characterize and Target p16high Cells In Vivo
Omori, S., Wang, T.-W., Johmura, Y., Kanai, T., Nakano, Y., Kido, T., Susaki, E. A., Nakajima, T., Shichino, S., Ueha, S., et al. (2020) · Cell Metabolism · doi:10.1016/j.cmet.2020.09.006 · Cited by 194
Therapeutic interventions for aging: the case of cellular senescence
Soto-Gamez, A., & Demaria, M. (2017) · Drug Discovery Today · doi:10.1016/j.drudis.2017.01.004 · Cited by 192
Cellular Senescence in Postmitotic Cells: Beyond Growth Arrest
Sapieha, P., & Mallette, F. A. (2018) · Trends in Cell Biology · doi:10.1016/j.tcb.2018.03.003 · Cited by 193
Tumor suppressor activity of the ERK/MAPK pathway by promoting selective protein degradation
Deschênes-Simard, X., Gaumont-Leclerc, M.-F., Bourdeau, V., Lessard, F., Moiseeva, O., Forest, V., Igelmann, S., Mallette, F. A., Saba-El-Leil, M. K., Meloche, S., et al. (2013) · Genes & Development · doi:10.1101/gad.203984.112 · Cited by 194
Histone variant H2A.J accumulates in senescent cells and promotes inflammatory gene expression
Contrepois, K., Coudereau, C., Benayoun, B. A., Schuler, N., Roux, P.-F., Bischof, O., Courbeyrette, R., Carvalho, C., Thuret, J.-Y., Ma, Z., et al. (2017) · Nature Communications · doi:10.1038/ncomms14995 · Cited by 191
Reducing Senescent Cell Burden in Aging and Disease
Pignolo, R. J., Passos, J. F., Khosla, S., Tchkonia, T., & Kirkland, J. L. (2020) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2020.03.005 · Cited by 177
Matias, I., Diniz, L. P., Damico, I. V., Araujo, A. P. B., Neves, L. D. S., Vargas, G., Leite, R. E. P., Suemoto, C. K., Nitrini, R., Jacob‐Filho, W., et al. (2022) · Aging Cell · doi:10.1111/acel.13521 · Cited by 183
Senescence in the pathogenesis of age-related macular degeneration
Blasiak, J. (2020) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-019-03420-x · Cited by 183
Loss of SATB1 Induces p21-Dependent Cellular Senescence in Post-mitotic Dopaminergic Neurons
Riessland, M., Kolisnyk, B., Kim, T. W., Cheng, J., Ni, J., Pearson, J. A., Park, E. J., Dam, K., Acehan, D., Ramos-Espiritu, L. S., et al. (2019) · Cell Stem Cell · doi:10.1016/j.stem.2019.08.013 · Cited by 180
Sentinel p16 INK4a+ cells in the basement membrane form a reparative niche in the lung
Reyes, N. S., Krasilnikov, M., Allen, N. C., Lee, J. Y., Hyams, B., Zhou, M., Ravishankar, S., Cassandras, M., Wang, C., Khan, I., et al. (2022) · Science · doi:10.1126/science.abf3326 · Cited by 181
Self-citationSenescence-induced inflammation: an important player and key therapeutic target in atherosclerosis
Stojanović, S. D., Fiedler, J., Bauersachs, J., Thum, T., & Sedding, D. G. (2020) · European Heart Journal · doi:10.1093/eurheartj/ehz919 · Cited by 188
HMGB2 orchestrates the chromatin landscape of senescence-associated secretory phenotype gene loci
Aird, K. M., Iwasaki, O., Kossenkov, A. V., Tanizawa, H., Fatkhutdinov, N., Bitler, B. G., Le, L., Alicea, G., Yang, T.-L., Johnson, F. B., et al. (2016) · Journal of Cell Biology · doi:10.1083/jcb.201608026 · Cited by 175
A Novel Indication for Panobinostat as a Senolytic Drug in NSCLC and HNSCC
Samaraweera, L., Adomako, A., Rodriguez-Gabin, A., & McDaid, H. M. (2017) · Scientific Reports · doi:10.1038/s41598-017-01964-1 · Cited by 183
Senescence in Wound Repair: Emerging Strategies to Target Chronic Healing Wounds
Wilkinson, H. N., & Hardman, M. J. (2020) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2020.00773 · Cited by 173
Spatial and Temporal Control of Senescence
Ito, Y., Hoare, M., & Narita, M. (2017) · Trends in Cell Biology · doi:10.1016/j.tcb.2017.07.004 · Cited by 178
Astrocyte senescence promotes glutamate toxicity in cortical neurons
Limbad, C., Oron, T. R., Alimirah, F., Davalos, A. R., Tracy, T. E., Gan, L., Desprez, P.-Y., & Campisi, J. (2020) · PLOS ONE · doi:10.1371/journal.pone.0227887 · Cited by 183
Self-citationParacrine roles of cellular senescence in promoting tumourigenesis
Gonzalez-Meljem, J. M., Apps, J. R., Fraser, H. C., & Martinez-Barbera, J. P. (2018) · British Journal of Cancer · doi:10.1038/s41416-018-0066-1 · Cited by 183
Astrocyte Senescence and Alzheimer’s Disease: A Review
Han, X., Zhang, T., Liu, H., Mi, Y., & Gou, X. (2020) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2020.00148 · Cited by 177
Bent, E. H., Gilbert, L. A., & Hemann, M. T. (2016) · Genes & Development · doi:10.1101/gad.284851.116 · Cited by 179
Obesity and hyperinsulinemia drive adipocytes to activate a cell cycle program and senesce
Li, Q., Hagberg, C. E., Silva Cascales, H., Lang, S., Hyvönen, M. T., Salehzadeh, F., Chen, P., Alexandersson, I., Terezaki, E., Harms, M. J., et al. (2021) · Nature Medicine · doi:10.1038/s41591-021-01501-8 · Cited by 178
Kirsner, R. S., Marston, W. A., Snyder, R. J., Lee, T. D., Cargill, D. I., & Slade, H. B. (2012) · The Lancet · doi:10.1016/s0140-6736(12)60644-8 · Cited by 172
PAI-1–regulated extracellular proteolysis governs senescence and survival in Klotho mice
Eren, M., Boe, A. E., Murphy, S. B., Place, A. T., Nagpal, V., Morales-Nebreda, L., Urich, D., Quaggin, S. E., Budinger, G. R. S., Mutlu, G. M., et al. (2014) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1321942111 · Cited by 176
Clearance of senescent cells during cardiac ischemia–reperfusion injury improves recovery
Dookun, E., Walaszczyk, A., Redgrave, R., Palmowski, P., Tual‐Chalot, S., Suwana, A., Chapman, J., Jirkovsky, E., Donastorg Sosa, L., Gill, E., et al. (2020) · Aging Cell · doi:10.1111/acel.13249 · Cited by 173
Lai, P., Liu, L., Bancaro, N., Troiani, M., Calì, B., Li, Y., Chen, J., Singh, P. K., Arzola, R. A., Attanasio, G., et al. (2025) · Immunity · doi:10.1016/j.immuni.2025.03.005 · Cited by 174
Noureddine, H., Gary-Bobo, G., Alifano, M., Marcos, E., Saker, M., Vienney, N., Amsellem, V., Maitre, B., Chaouat, A., Chouaid, C., et al. (2011) · Circulation Research · doi:10.1161/circresaha.111.241299 · Cited by 173
Senescence in Post-Mitotic Cells: A Driver of Aging?
von Zglinicki, T., Wan, T., & Miwa, S. (2021) · Antioxidants & Redox Signaling · doi:10.1089/ars.2020.8048 · Cited by 170
SIRT1 suppresses the senescence-associated secretory phenotype through epigenetic gene regulation
Hayakawa, T., Iwai, M., Aoki, S., Takimoto, K., Maruyama, M., Maruyama, W., & Motoyama, N. (2015) · PLOS ONE · doi:10.1371/journal.pone.0116480 · Cited by 170
“Social Life” of Senescent Cells: What Is SASP and Why Study It?
Borodkina, A. V., Deryabin, P. I., Giukova, А. А., & Nikolsky, N. N. (2018) · Acta Naturae · doi:10.32607/20758251-2018-10-1-4-14 · Cited by 170
Galactose‐modified duocarmycin prodrugs as senolytics
Guerrero, A., Guiho, R., Herranz, N., Uren, A., Withers, D. J., Martínez‐Barbera, J. P., Tietze, L. F., & Gil, J. (2020) · Aging Cell · doi:10.1111/acel.13133 · Cited by 172
Elzi, D. J., Lai, Y., Song, M., Hakala, K., Weintraub, S. T., & Shiio, Y. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1120437109 · Cited by 154
T-cell aging in rheumatoid arthritis
Weyand, C. M., Yang, Z., & Goronzy, J. J. (2014) · Current Opinion in Rheumatology · doi:10.1097/bor.0000000000000011 · Cited by 164
Expression of p16INK4a is a biomarker of chondrocyte aging but does not cause osteoarthritis
Diekman, B. O., Sessions, G. A., Collins, J. A., Knecht, A. K., Strum, S. L., Mitin, N. K., Carlson, C. S., Loeser, R. F., & Sharpless, N. E. (2018) · Aging Cell · doi:10.1111/acel.12771 · Cited by 158
Perrott, K. M., Wiley, C. D., Desprez, P.-Y., & Campisi, J. (2017) · GeroScience · doi:10.1007/s11357-017-9970-1 · Cited by 163
Self-citationMechanism and therapeutic potential of targeting cGAS-STING signaling in neurological disorders
Huang, Y., Liu, B., Sinha, S. C., Amin, S., & Gan, L. (2023) · Molecular Neurodegeneration · doi:10.1186/s13024-023-00672-x · Cited by 164
Discovery, development, and future application of senolytics: theories and predictions
Wissler Gerdes, E. O., Zhu, Y., Tchkonia, T., & Kirkland, J. L. (2020) · The FEBS Journal · doi:10.1111/febs.15264 · Cited by 160
Apoptosis and aging: increased resistance to apoptosis enhances the aging process
Salminen, A., Ojala, J., & Kaarniranta, K. (2011) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-010-0597-y · Cited by 158
Histone Acetyltransferase p300 Induces De Novo Super-Enhancers to Drive Cellular Senescence
Sen, P., Lan, Y., Li, C. Y., Sidoli, S., Donahue, G., Dou, Z., Frederick, B., Chen, Q., Luense, L. J., Garcia, B. A., et al. (2019) · Molecular Cell · doi:10.1016/j.molcel.2019.01.021 · Cited by 164
p53 isoforms regulate aging- and tumor-associated replicative senescence in T lymphocytes
Mondal, A. M., Horikawa, I., Pine, S. R., Fujita, K., Morgan, K. M., Vera, E., Mazur, S. J., Appella, E., Vojtesek, B., Blasco, M. A., et al. (2013) · Journal of Clinical Investigation · doi:10.1172/jci70355 · Cited by 164
Elimination of p19ARF-expressing cells enhances pulmonary function in mice
Hashimoto, M., Asai, A., Kawagishi, H., Mikawa, R., Iwashita, Y., Kanayama, K., Sugimoto, K., Sato, T., Maruyama, M., & Sugimoto, M. (2016) · JCI Insight · doi:10.1172/jci.insight.87732 · Cited by 162
DNA damage response (DDR) and senescence: shuttled inflamma-miRNAs on the stage of inflamm-aging
Olivieri, F., Albertini, M. C., Orciani, M., Ceka, A., Cricca, M., Procopio, A. D., & Bonafè, M. (2015) · Oncotarget · doi:10.18632/oncotarget.5899 · Cited by 163
Senescence and senotherapeutics: a new field in cancer therapy
Myrianthopoulos, V., Evangelou, K., Vasileiou, P. V. S., Cooks, T., Vassilakopoulos, T. P., Pangalis, G. A., Kouloukoussa, M., Kittas, C., Georgakilas, A. G., & Gorgoulis, V. G. (2019) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2018.08.006 · Cited by 160
Yoshida, S., Nakagami, H., Hayashi, H., Ikeda, Y., Sun, J., Tenma, A., Tomioka, H., Kawano, T., Shimamura, M., Morishita, R., et al. (2020) · Nature Communications · doi:10.1038/s41467-020-16347-w · Cited by 161
MLL1 is essential for the senescence-associated secretory phenotype
Capell, B. C., Drake, A. M., Zhu, J., Shah, P. P., Dou, Z., Dorsey, J., Simola, D. F., Donahue, G., Sammons, M., Rai, T. S., et al. (2016) · Genes & Development · doi:10.1101/gad.271882.115 · Cited by 156
Prattichizzo, F., De Nigris, V., Mancuso, E., Spiga, R., Giuliani, A., Matacchione, G., Lazzarini, R., Marcheselli, F., Recchioni, R., Testa, R., et al. (2018) · Redox Biology · doi:10.1016/j.redox.2017.12.001 · Cited by 159
Cell Senescence, DNA Damage, and Metabolism
Shmulevich, R., & Krizhanovsky, V. (2021) · Antioxidants & Redox Signaling · doi:10.1089/ars.2020.8043 · Cited by 157
Yu, Y., Schleich, K., Yue, B., Ji, S., Lohneis, P., Kemper, K., Silvis, M. R., Qutob, N., van Rooijen, E., Werner-Klein, M., et al. (2018) · Cancer Cell · doi:10.1016/j.ccell.2018.01.002 · Cited by 156
Epigenetic clock analyses of cellular senescence and ageing.
Lowe, D., Horvath, S., & Raj, K. (2016) · Oncotarget · doi:10.18632/oncotarget.7383 · Cited by 147
Lee, K. S., Lin, S., Copland, D. A., Dick, A. D., & Liu, J. (2021) · Journal of Neuroinflammation · doi:10.1186/s12974-021-02088-0 · Cited by 150
Cellular senescence impairs the reversibility of pulmonary arterial hypertension
van der Feen, D. E., Bossers, G. P. L., Hagdorn, Q. A. J., Moonen, J.-R., Kurakula, K., Szulcek, R., Chappell, J., Vallania, F., Donato, M., Kok, K., et al. (2020) · Science Translational Medicine · doi:10.1126/scitranslmed.aaw4974 · Cited by 150
The role of cellular senescence and SASP in tumour microenvironment
Takasugi, M., Yoshida, Y., Hara, E., & Ohtani, N. (2023) · The FEBS Journal · doi:10.1111/febs.16381 · Cited by 144
Placental membrane aging and HMGB1 signaling associated with human parturition
Menon, R., Behnia, F., Polettini, J., Saade, G. R., Campisi, J., & Velarde, M. (2016) · Aging · doi:10.18632/aging.100891 · Cited by 143
Self-citationTargeted Reduction of Senescent Cell Burden Alleviates Focal Radiotherapy-Related Bone Loss
Chandra, A., Lagnado, A. B., Farr, J. N., Monroe, D. G., Park, S., Hachfeld, C., Tchkonia, T., Kirkland, J. L., Khosla, S., Passos, J. F., et al. (2020) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.3978 · Cited by 138
Biomarkers to identify and isolate senescent cells
Matjusaitis, M., Chin, G., Sarnoski, E. A., & Stolzing, A. (2016) · Ageing Research Reviews · doi:10.1016/j.arr.2016.05.003 · Cited by 144
Stromal-Initiated Changes in the Bone Promote Metastatic Niche Development
Luo, X., Fu, Y., Loza, A. J., Murali, B., Leahy, K. M., Ruhland, M. K., Gang, M., Su, X., Zamani, A., Shi, Y., et al. (2016) · Cell Reports · doi:10.1016/j.celrep.2015.12.016 · Cited by 141
Role of the inflammation-autophagy-senescence integrative network in osteoarthritis
Vinatier, C., Domínguez, E., Guicheux, J., & Caramés, B. (2018) · Frontiers in Physiology · doi:10.3389/fphys.2018.00706 · Cited by 135
Discovery of senolytics using machine learning
Smer-Barreto, V., Quintanilla, A., Elliott, R. J. R., Dawson, J. C., Sun, J., Campa, V. M., Lorente-Macías, Á., Unciti-Broceta, A., Carragher, N. O., Acosta, J. C., et al. (2023) · Nature Communications · doi:10.1038/s41467-023-39120-1 · Cited by 139
Gene expression profiling of replicative and induced senescence
Purcell, M., Kruger, A., & Tainsky, M. A. (2014) · Cell Cycle · doi:10.4161/15384101.2014.973327 · Cited by 132
The Chromatin Landscape of Cellular Senescence
Criscione, S. W., Teo, Y. V., & Neretti, N. (2016) · Trends in Genetics · doi:10.1016/j.tig.2016.09.005 · Cited by 137
DNA damage drives accelerated bone aging via an NF- κ B–dependent mechanism
Chen, Q., Liu, K., Robinson, A. R., Clauson, C. L., Blair, H. C., Robbins, P. D., Niedernhofer, L. J., & Ouyang, H. (2013) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.1851 · Cited by 135
NADPH Oxidases and Mitochondria in Vascular Senescence
Salazar, G. (2018) · International Journal of Molecular Sciences · doi:10.3390/ijms19051327 · Cited by 133
Cellular senescence links aging and diabetes in cardiovascular disease
Shakeri, H., Lemmens, K., Gevaert, A. B., De Meyer, G. R. Y., & Segers, V. F. M. (2018) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00287.2018 · Cited by 134
Carroll, J. E., Cole, S. W., Seeman, T. E., Breen, E. C., Witarama, T., Arevalo, J. M. G., Ma, J., & Irwin, M. R. (2016) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2015.08.024 · Cited by 129
Sanz-Ros, J., Romero-García, N., Mas-Bargues, C., Monleón, D., Gordevicius, J., Brooke, R. T., Dromant, M., Díaz, A., Derevyanko, A., Guío-Carrión, A., et al. (2022) · Science Advances · doi:10.1126/sciadv.abq2226 · Cited by 131
Gonzalez-Meljem, J. M., Haston, S., Carreno, G., Apps, J. R., Pozzi, S., Stache, C., Kaushal, G., Virasami, A., Panousopoulos, L., Mousavy-Gharavy, S. N., et al. (2017) · Nature Communications · doi:10.1038/s41467-017-01992-5 · Cited by 130
Role of Cellular Senescence in Type II Diabetes
Narasimhan, A., Flores, R. R., Robbins, P. D., & Niedernhofer, L. J. (2021) · Endocrinology · doi:10.1210/endocr/bqab136 · Cited by 133
Cortical neurons develop a senescence-like phenotype promoted by dysfunctional autophagy
Moreno-Blas, D., Gorostieta-Salas, E., Pommer-Alba, A., Muciño-Hernández, G., Gerónimo-Olvera, C., Maciel-Barón, L. A., Konigsberg, M., Massieu, L., & Castro-Obregón, S. (2019) · Aging · doi:10.18632/aging.102181 · Cited by 128
Stout, M. B., Steyn, F. J., Jurczak, M. J., Camporez, J.-P. G., Zhu, Y., Hawse, J. R., Jurk, D., Palmer, A. K., Xu, M., Pirtskhalava, T., et al. (2017) · The Journals of Gerontology Series A: Biological Sciences and Medical Sciences · doi:10.1093/gerona/glv309 · Cited by 119
Recent advances in the discovery of senolytics
Zhang, L., Pitcher, L. E., Prahalad, V., Niedernhofer, L. J., & Robbins, P. D. (2021) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2021.111587 · Cited by 115
Senolytics for Cancer Therapy: Is All that Glitters Really Gold?
Carpenter, V. J., Saleh, T., & Gewirtz, D. A. (2021) · Cancers · doi:10.3390/cancers13040723 · Cited by 124
From cellular senescence to Alzheimer’s disease: The role of telomere shortening
Boccardi, V., Pelini, L., Ercolani, S., Ruggiero, C., & Mecocci, P. (2015) · Ageing Research Reviews · doi:10.1016/j.arr.2015.04.003 · Cited by 121
Age- and tissue-specific expression of senescence biomarkers in mice.
Hudgins, A. D., Tazearslan, C., Tare, A., Zhu, Y., Huffman, D., & Suh, Y. (2018) · Frontiers in Genetics · doi:10.3389/fgene.2018.00059 · Cited by 124
Small-molecule MDM2 antagonists attenuate the senescence-associated secretory phenotype
Wiley, C. D., Schaum, N., Alimirah, F., Lopez-Dominguez, J. A., Orjalo, A. V., Scott, G., Desprez, P.-Y., Benz, C., Davalos, A. R., & Campisi, J. (2018) · Scientific Reports · doi:10.1038/s41598-018-20000-4 · Cited by 124
Self-citationBurton, D. G. A., Matsubara, H., & Ikeda, K. (2010) · Experimental Gerontology · doi:10.1016/j.exger.2010.07.005 · Cited by 121
Senescent Carcinoma-Associated Fibroblasts Upregulate IL8 to Enhance Prometastatic Phenotypes
Wang, T., Notta, F., Navab, R., Joseph, J., Ibrahimov, E., Xu, J., Zhu, C.-Q., Borgida, A., Gallinger, S., & Tsao, M.-S. (2017) · Molecular Cancer Research · doi:10.1158/1541-7786.mcr-16-0192 · Cited by 123
Zhao, J., Zhang, L., Lu, A., Han, Y., Colangelo, D., Bukata, C., Scibetta, A., Yousefzadeh, M. J., Li, X., Gurkar, A. U., et al. (2020) · Aging · doi:10.18632/aging.102863 · Cited by 122
Ali, D., Tencerova, M., Figeac, F., Kassem, M., & Jafari, A. (2022) · Frontiers in Endocrinology · doi:10.3389/fendo.2022.981487 · Cited by 122
Amnion-Epithelial-Cell-Derived Exosomes Demonstrate Physiologic State of Cell under Oxidative Stress
Sheller, S., Papaconstantinou, J., Urrabaz-Garza, R., Richardson, L., Saade, G., Salomon, C., & Menon, R. (2016) · PLOS ONE · doi:10.1371/journal.pone.0157614 · Cited by 121
Cellular senescence, senescence-associated secretory phenotype, and chronic kidney disease
Wang, W.-J., Cai, G.-Y., & Chen, X.-M. (2017) · Oncotarget · doi:10.18632/oncotarget.17327 · Cited by 121
Pharmacological CDK4/6 inhibition reveals a p53‐dependent senescent state with restricted toxicity
Wang, B., Varela‐Eirin, M., Brandenburg, S. M., Hernandez‐Segura, A., van Vliet, T., Jongbloed, E. M., Wilting, S. M., Ohtani, N., Jager, A., & Demaria, M. (2022) · The EMBO Journal · doi:10.15252/embj.2021108946 · Cited by 113
Kandhaya‐Pillai, R., Yang, X., Tchkonia, T., Martin, G. M., Kirkland, J. L., & Oshima, J. (2022) · Aging Cell · doi:10.1111/acel.13646 · Cited by 119
Chandra, A., Lagnado, A. B., Farr, J. N., Doolittle, M., Tchkonia, T., Kirkland, J. L., LeBrasseur, N. K., Robbins, P. D., Niedernhofer, L. J., Ikeno, Y., et al. (2022) · Aging Cell · doi:10.1111/acel.13602 · Cited by 120
The impact of senescence-associated T cells on immunosenescence and age-related disorders
Fukushima, Y., Minato, N., & Hattori, M. (2018) · Inflammation and Regeneration · doi:10.1186/s41232-018-0082-9 · Cited by 118
Dagouassat, M., Gagliolo, J.-M., Chrusciel, S., Bourin, M.-C., Duprez, C., Caramelle, P., Boyer, L., Hue, S., Stern, J.-B., Validire, P., et al. (2013) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/rccm.201208-1361oc · Cited by 120
Implicating endothelial cell senescence to dysfunction in the ageing and diseased brain
Graves, S. I., & Baker, D. J. (2020) · Basic & Clinical Pharmacology & Toxicology · doi:10.1111/bcpt.13403 · Cited by 118
Lau, L., Porciuncula, A., Yu, A., Iwakura, Y., & David, G. (2019) · Molecular and Cellular Biology · doi:10.1128/mcb.00586-18 · Cited by 119
Cellular senescence in aging and age-related diseases: Implications for neurodegenerative diseases
(2020) · International Review of Neurobiology · doi:10.1016/bs.irn.2020.03.019 · Cited by 114
Paramos-de-Carvalho, D., Jacinto, A., & Saúde, L. (2021) · eLife · doi:10.7554/elife.72449 · Cited by 111
Antignano, I., Liu, Y., Offermann, N., & Capasso, M. (2023) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-023-04775-y · Cited by 117
Shivshankar, P., Boyd, A. R., Le Saux, C. J., Yeh, I., & Orihuela, C. J. (2011) · Aging Cell · doi:10.1111/j.1474-9726.2011.00720.x · Cited by 117
Are there roles for brain cell senescence in aging and neurodegenerative disorders?
Tan, F. C. C., Hutchison, E. R., Eitan, E., & Mattson, M. P. (2014) · Biogerontology · doi:10.1007/s10522-014-9532-1 · Cited by 116
Thapa, R. K., Nguyen, H. T., Jeong, J.-H., Kim, J. R., Choi, H.-G., Yong, C. S., & Kim, J. O. (2017) · Scientific Reports · doi:10.1038/srep43299 · Cited by 115
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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