The DOI matches its Crossref record; 31 of the 31 references it cites were found in a registry or an index.
Persistent DNA damage signalling triggers senescence-associated inflammatory cytokine secretion
Open accessAbstract
Cellular senescence suppresses cancer by stably arresting the proliferation of damaged cells. Paradoxically, senescent cells also secrete factors that alter tissue microenvironments. The pathways regulating this secretion are unknown. We show that damaged human cells develop persistent chromatin lesions bearing hallmarks of DNA double-strand breaks (DSBs), which initiate increased secretion of inflammatory cytokines such as interleukin-6 (IL-6). Cytokine secretion occurred only after establishment of persistent DNA damage signalling, usually associated with senescence, not after transient DNA damage responses (DDRs). Initiation and maintenance of this cytokine response required the DDR proteins ATM, NBS1 and CHK2, but not the cell-cycle arrest enforcers p53 and pRb. ATM was also essential for IL-6 secretion during oncogene-induced senescence and by damaged cells that bypass senescence. Furthermore, DDR activity and IL-6 were elevated in human cancers, and ATM-depletion suppressed the ability of senescent cells to stimulate IL-6-dependent cancer cell invasiveness. Thus, in addition to orchestrating cell-cycle checkpoints and DNA repair, a new and important role of the DDR is to allow damaged cells to communicate their compromised state to the surrounding tissue.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Many such stressors activate DNA damage response signaling and activation of the p53/p21CIP1/WAF1, p16INK4a/retinoblastoma protein or other pathways, resulting in cell cycle arrest and the development of a senescence-associated secretory phenotype (SASP)24,40,48−53”
From Cellular senescence and senolytics: the path to the clinic (2022) · cites this paper as [50]
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
“Nevertheless, there is substantial overlap among SASPs; proinflammatory cytokines are the most highly conserved feature, cutting across many different cell types and senescence-inducing stimuli (33, 42, 96, 99, 100, 112–114).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [42]
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 primarily a property of cells that senesce owing to, or accompanied by, genomic damage or epigenomic perturbation.”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [42]
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
“These nuclear structures contain the activated DDR proteins that ensure the persistent DDR signaling (43) that is needed for both the senescence growth arrest and the SASP (32, 42, 43).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [42]
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
“Of particular importance, these DDR proteins stimulate the SASP only after persistent DDR signaling has been established.”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [42]
Experimental — accuracy not yet measured
The 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, p53 inactivation in cells that do not express p16INK4a, which renders the senescence growth arrest irreversible (10), causes cells to resume proliferation, but the SASP remains active (32, 42).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [42]
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
“That is, the rapid robust DDR that occurs immediately after DNA damage does not induce a SASP; rather, the SASP develops slowly—over several days in culture—and only after the initial DDR subsides (32, 42).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [42]
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
“Many, but not all, SASP components are positively regulated by the DDR proteins ATM, NBS1 (Nijmegen breakage syndrome 1), and CHK2 (checkpoint kinase 2) (42, 67).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [42]
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
“In contrast, cells that senesce owing to DNA damage, dysfunctional telomeres, epigenomic disruption, mitogenic signals, oxidative stress, and other senescence-inducing stimuli develop a SASP of varying qualities and robustness (32, 33, 42, 67, 94, 96, 99, 100, 112–114).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [42]
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
“ATM, NBS1 and CHK2 prime SASP genes for activation, as depletion of these DDR upstream regulators dampens cytokine production in response to genotoxic stress86”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [86]
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
“Because p53 also limits SASP gene expression (Coppé et al., 2008; Rodier et al., 2009), we depleted p53 in WT and rho0 cells and measured IL1A and IL1B mRNA levels.”
From Mitochondrial Dysfunction Induces Senescence with a Distinct Secretory Phenotype (2016) · cites this paper as Rodier et al., 2009
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
“IR robustly activates p53, which subsides to a low chronic level in 7–10 days as the SASP develops (Coppé et al., 2008; Rodier et al., 2009).”
From Mitochondrial Dysfunction Induces Senescence with a Distinct Secretory Phenotype (2016) · cites this paper as Rodier et al., 2009
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
“A signature pro-inflammatory secretory phenotype takes 7–10 days to develop under DDR (Coppe et al, 2008; Rodier et al, 2009).”
From Feedback between p21 and reactive oxygen production is necessary for cell senescence (2010) · cites this paper as Rodier et al, 2009
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
“Own (Supplementary Figure S1A) and published (Coppe et al, 2008; Rodier et al, 2009) data indicated that a full senescent phenotype develops over 7–10 days in human fibroblasts.”
From Feedback between p21 and reactive oxygen production is necessary for cell senescence (2010) · cites this paper as Rodier et al, 2009
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 [27]
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
“In addition, expression of the CDK inhibitors p16 or p21 leads to the induction of senescence without the development of a DDR; this senescent phenotype lacks a proinflammatory SASP (Rodier et al. 2009).”
From Cellular senescence and its effector programs (2014) · cites this paper as Rodier et al. 2009
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
“Loss of ataxia telangiectasia-mutated (ATM) or other factors responding to DNA damage (such as NBS1 and CHK2) leads to reductions in some SASP factors, such as IL6 and IL8, central components of SASP, during not only DDR-induced senescence but also OIS (Rodier et al. 2009).”
From Cellular senescence and its effector programs (2014) · cites this paper as Rodier et al. 2009
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
“Induction of p21 and a Notch- driven SASP are considered early events 70,75,76 , whereas upregulation of p16 INK4a and an NF- κB- driven SASP are evident at later stages of senescence 71,77,78 .”
From Senescence and cancer — role and therapeutic opportunities (2022) · cites this paper as [78]
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
“Alkylating agents 27,95,96 (for example, cisplatin, cyclophosphamide and temozolomide), topoisomerase inhibitors 27,65,91,95 (such as doxorubicin, etoposide and camptothecin) and γ- irradiation 78 , but also microtubule inhibitors 27,97,98 (for example, paclitaxel) and, to a lesser extent, vinca alkaloids 78 (for example, vincristine), have all been identified as senescence inducers in preclinical”
From Senescence and cancer — role and therapeutic opportunities (2022) · cites this paper as [78]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“In contrast to positive regulation by the DDR, p53 negatively regulates or, more accurately, restrains the SASP (32, 42) (Figure 2).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [42]
The cited source says what the claim attributes to it.
In the citing paper
“SASP is both promoted by DDR13 and can promote DDR and TAF formation in an autocrine and paracrine fashion14–16.”
From Telomere dysfunction in ageing and age-related diseases (2022) · cites this paper as [13]
The cited source says what the claim attributes to it.
In the citing paper
“Inhibition of p53 has the opposite effect, as it further enhances SASP following a senescence-inducing insult86, which may contribute to the generation of an inflammatory microenvironment that favours senescence escape and malignant transformation”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [86]
The cited source says what the claim attributes to it.
In the citing paper
“persistent DDR signalling is often required to initiate inflammatory cytokine secretion86”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [86]
The cited source says what the claim attributes to it.
In the citing paper
“Persistent DDR activity is required for the induction of several proinflammatory SASP factors, such as IL-6 and IL-8 (Rodier et al. 2009).”
From Senescence and the SASP: many therapeutic avenues (2020) · cites this paper as Rodier et al. 2009
The cited source says what the claim attributes to it.
In the citing paper
“Furthermore, dysfunctional mitochondria,195 persistent DNA damage response,196 CCAAT/enhancer-binding protein β (C/EBPβ) and NF-κB,197 mTOR, and other factors are involved in regulating SASP.194”
From Inflammation and aging: signaling pathways and intervention therapies (2023) · cites this paper as [196]
The cited source says what the claim attributes to it.
In the citing paper
“Senescent cells induced by either genotoxic stress, replicative exhaustion, or oncogenic stress secrete myriad factors associated with inflammation, proliferation, and modulation of the extracellular matrix (ECM) (Acosta et al. 2008; Kuilman et al. 2008; Rodier et al. 2009).”
From Cellular senescence and its effector programs (2014) · cites this paper as Rodier et al. 2009
The cited source says what the claim attributes to it.
In the citing paper
“Of note, DDR-independent senescence has also been reported in some experimental conditions where p16, p38MAPK, or ATR is constitutively activated or tumor suppressor Pten is completely lost (Toledo et al. 2008; Rodier et al. 2009; Alimonti et al. 2010; Freund et al. 2011).”
From Cellular senescence and its effector programs (2014) · cites this paper as Rodier et al. 2009
In the citing paper
“Senescent cells remain viable, have alterations in metabolic activity and undergo dramatic changes in gene expression and develop a complex senescence-associated secretory phenotype.”
From Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021) · cites this paper as Rodier et al., 2009
In the citing paper
“They undergo dramatic gene expression changes along with chromatin remodeling and engagement of a persistent DNA damage response (DDR) (Rodier et al., 2009; Wang et al., 2009; Sulli et al., 2012; Chandra et al., 2015).”
From Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021) · cites this paper as Rodier et al., 2009
In the citing paper
“DNA damage, dysfunctional telomeres, genomic damage, epigenomic perturbation, mitogenic proliferative signals, oxidative stress or other senescence-inducing stimuli, all leading to prolonged DDR express SASP to different extents (Acosta et al., 2008; Kuilman et al., 2008; Rodier et al., 2009; Coppé et al., 2010b; Pazolli et al., 2012).”
From Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021) · cites this paper as Rodier et al., 2009
In the citing paper
“In general terms, DNA damage activates DDR, a p53/21-dependent response that is originally transient but which can become persistent if the damage is severe enough, and which can also be reversed through the p16/pRB pathways [219], [241].”
From Redox control of senescence and age-related disease. (2017) · cites this paper as [241]
In the citing paper
“the SASP does not depend on either p53 or p16INK4a, which suggests that it is controlled by an independent branch of the senescence regulatory network (2, 10, 20, 26).”
From The DNA damage response induces inflammation and senescence by inhibiting autophagy of GATA4. (2015) · cites this paper as [20]
In the citing paper
“However, senescent cells acquire a “senescence-associated secretory phenotype” (SASP), secreting many pro-inflammatory cytokines, proteases, and growth and angiogenesis factors that can disrupt microenvironments and compromise tissue structure and function thereby contributing to local and systemic ageing-associated pathologies47 and promote cancer64.”
From The central role of DNA damage in the ageing process (2021) · cites this paper as [47]
In the citing paper
“although cellular senescence in vitro may also occur without detectable DDR [31,32].”
From Ageing, Cellular Senescence and Neurodegenerative Disease (2018) · cites this paper as [32]
In the citing paper
“In addition, tumor cells activate the PKA-CREB and P38 pathways by producing cAMP, thereby causing DNA damage and senescence of T cells [51, 53, 58–63].”
From Immunosenescence: a key player in cancer development (2020) · cites this paper as [62]
In the citing paper
“Cell cycle controlling proteins p16, p21, and p53, normally inhibit cell cycle progression and have been shown to be accumulated in senescent cells [49–51].”
From T cell anergy, exhaustion, senescence, and stemness in the tumor microenvironment (2013) · cites this paper as [50]
In the citing paper
“Cellular senescence is a primary aging process and tumor suppressive mechanism characterized by irreversible growth arrest, apoptosis resistance, production of a senescence-associated secretory phenotype (SASP), mitochondrial dysfunction, and alterations in DNA and chromatin.”
From Reducing Senescent Cell Burden in Aging and Disease (2020) · cites this paper as [22]
In the citing paper
“Hallmarks of the cellular senescence phenotype include irreversible growth arrest, a senescence-associated secretory phenotype (SASP) (Box 1), apoptosis resistance, mitochondrial dysfunction [21], persistent DNA damage foci [22] and epigenetic remodeling, which includes formation of senescence-associated heterochromatin foci [23].”
From Reducing Senescent Cell Burden in Aging and Disease (2020) · cites this paper as [22]
In the citing paper
“The p53-dependence of CCL2 production may distinguish CCL2 from some of the other chemokines produced in senescent cells, which are dependent on the senescent state but are produced independently of p53 (Coppé et al., 2008; Rodier et al., 2009).”
From p53-dependent chemokine production by senescent tumor cells supports NKG2D-dependent tumor elimination by natural killer cells (2013) · cites this paper as Rodier et al., 2009
In the citing paper
“Senescent cells secrete a distinct suite of inflammatory cytokines and chemokines depending upon whether senescence is induced by genotoxic stress, [23] or mitochondrial dysfunction, as in the form of deficiencies in mitochondrial sirtuins or damage to mitochondrial DNA [24]”
From Aging of the immune system: Focus on inflammation and vaccination (2016) · cites this paper as [23]
In the citing paper
“In addition to the downregulation of cell cycle genes, senescent cells are programmed to secrete different chemokines, pro-inflammatory cytokines, growth factors, and matrix-remodeling enzymes that define the SASP [136,147,148].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [148]
In the citing paper
“Activation of the SASP program requires a sustained DDR signal but is independent of p53, p21, and p16 (the mediators of cell cycle arrest in senescent cells) [147,148].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [148]
In the citing paper
“ATM signaling does not regulate the entire production of SASP factors, although it is required for the secretion of IL-6 and IL-8, the most conserved and robustly expressed inflammatory cytokines [148].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [148]
In the citing paper
“SASP factor production requires continuous DNA damage signaling [148].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [148]
In the citing paper
“the secretome of senescent tumor cells can also drive tumor progression by promoting inflammation and potentially stimulating the growth and invasiveness of nearby tumor cells [148,154,163].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [148]
In the citing paper
“DNA damage is a potent activator of inflammatory signaling and senescence (Coppé et al, 2008; Rodier et al, 2009; Brzostek‐Racine et al, 2011; Härtlova et al, 2015).”
From Mechanisms of DNA damage-mediated neurotoxicity in neurodegenerative disease (2022) · cites this paper as Rodier et al, 2009
In the citing paper
“Initially, induction of persistent DDR signaling in cell cultures including fibroblasts (Coppé et al, 2008; Rodier et al, 2009), bone marrow‐derived macrophages (BMDMs) (Härtlova et al, 2015), and primary monocytes (Brzostek‐Racine et al, 2011) was found to elicit the SASP (Coppé et al, 2008).”
From Mechanisms of DNA damage-mediated neurotoxicity in neurodegenerative disease (2022) · cites this paper as Rodier et al, 2009
In the citing paper
“This secretory profile was found to be at least partially ATM‐dependent, implying the importance of DSB repair specifically in immune activation (Rodier et al, 2009; Brzostek‐Racine et al, 2011).”
From Mechanisms of DNA damage-mediated neurotoxicity in neurodegenerative disease (2022) · cites this paper as Rodier et al, 2009
In the citing paper
“These SASP factors are part of the IL-1-dependent inflammatory arm57, and are normally expressed by DNA damage-induced senescent cells.”
From Algorithmic assessment of cellular senescence in experimental and clinical specimens (2021) · cites this paper as [57]
In the citing paper
“These SASP factors are part of the IL-1-dependent inflammatory arm57, and are normally expressed by DNA damage-induced senescent cells.”
From Algorithmic assessment of cellular senescence in experimental and clinical specimens (2021) · cites this paper as [57]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
The limited in vitro lifetime of human diploid cell strains
Hayflick, L. (1965) · Experimental Cell Research · doi:10.1016/0014-4827(65)90211-9 · Cited by 5,876
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-citationA DNA damage checkpoint response in telomere-initiated senescence
Fagagna, F. D. D., Reaper, P. M., Clay-Farrace, L., Fiegler, H., Carr, P., von Zglinicki, T., Saretzki, G., Carter, N. P., & Jackson, S. P. (2003) · Nature · doi:10.1038/nature02118 · Cited by 2,917
DNA damage response as a candidate anti-cancer barrier in early human tumorigenesis
Bartkova, J., Hořejší, Z., Koed, K., Krämer, A., Tort, F., Zieger, K., Guldberg, P., Sehested, M., Nesland, J. M., Lukas, C., et al. (2005) · Nature · doi:10.1038/nature03482 · Cited by 2,688
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-citationOncogene-Induced Senescence Relayed by an Interleukin-Dependent Inflammatory Network
Kuilman, T., Michaloglou, C., Vredeveld, L. C. W., Douma, S., van Doorn, R., Desmet, C. J., Aarden, L. A., Mooi, W. J., & Peeper, D. S. (2008) · Cell · doi:10.1016/j.cell.2008.03.039 · Cited by 2,086
Senescence of Activated Stellate Cells Limits Liver Fibrosis
Krizhanovsky, V., Yon, M., Dickins, R. A., Hearn, S., Simon, J., Miething, C., Yee, H., Zender, L., & Lowe, S. W. (2008) · Cell · doi:10.1016/j.cell.2008.09.015 · Cited by 2,027
Activation of the DNA damage checkpoint and genomic instability in human precancerous lesions
Gorgoulis, V. G., Vassiliou, L.-V. F., Karakaidos, P., Zacharatos, P., Kotsinas, A., Liloglou, T., Venere, M., DiTullio, R. A., Kastrinakis, N. G., Levy, B., et al. (2005) · Nature · doi:10.1038/nature03485 · Cited by 2,009
Oncogene-induced senescence is part of the tumorigenesis barrier imposed by DNA damage checkpoints
Bartkova, J., Rezaei, N., Liontos, M., Karakaidos, P., Kletsas, D., Issaeva, N., Vassiliou, L.-V. F., Kolettas, E., Niforou, K., Zoumpourlis, V. C., et al. (2006) · Nature · doi:10.1038/nature05268 · Cited by 1,986
Flagged first, then by citations
Cited by
Sorted by citations
Immunity, Inflammation, and Cancer
Grivennikov, S. I., Greten, F. R., & Karin, M. (2010) · Cell · doi:10.1016/j.cell.2010.01.025 · Cited by 10,755
The senescence-associated secretory phenotype: the dark side of tumor suppression
Coppé, J.-P., Desprez, P.-Y., Krtolica, A., & Campisi, J. (2010) · Annual Review of Pathology: Mechanisms of Disease · doi:10.1146/annurev-pathol-121808-102144 · Cited by 5,206
Self-citationAging, Cellular Senescence, and Cancer
Campisi, J. (2013) · Annual Review of Physiology · doi:10.1146/annurev-physiol-030212-183653 · Cited by 2,954
Self-citationThe 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
The essence of senescence: Figure 1.
Kuilman, T., Michaloglou, C., Mooi, W. J., & Peeper, D. S. (2010) · Genes & Development · doi:10.1101/gad.1971610 · Cited by 2,038
Four faces of cellular senescence
Rodier, F., & Campisi, J. (2011) · Journal of Cell Biology · doi:10.1083/jcb.201009094 · Cited by 2,070
Self-citationCellular senescence and the senescent secretory phenotype: therapeutic opportunities
Tchkonia, T., Zhu, Y., van Deursen, J., Campisi, J., & Kirkland, J. L. (2013) · Journal of Clinical Investigation · doi:10.1172/jci64098 · Cited by 1,774
Self-citationDebacq-Chainiaux, F., Erusalimsky, J. D., Campisi, J., & Toussaint, O. (2009) · Nature Protocols · doi:10.1038/nprot.2009.191 · Cited by 1,668
Self-citationMechanisms 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
Mitotic progression following DNA damage enables pattern recognition within micronuclei
Harding, S. M., Benci, J. L., Irianto, J., Discher, D. E., Minn, A. J., & Greenberg, R. A. (2017) · Nature · doi:10.1038/nature23470 · Cited by 1,508
Baar, M. P., Brandt, R. M. C., Putavet, D. A., Klein, J. D. D., Derks, K. W. J., Bourgeois, B. R. M., Stryeck, S., Rijksen, Y., van Willigenburg, H., Feijtel, D. A., et al. (2017) · Cell · doi:10.1016/j.cell.2017.02.031 · Cited by 1,454
Self-citationInflammation and aging: signaling pathways and intervention therapies
Li, X., Li, C., Zhang, W., Wang, Y., Qian, P., & Huang, H. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01502-8 · Cited by 1,443
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-citationFrom discoveries in ageing research to therapeutics for healthy ageing
Campisi, J., Kapahi, P., Lithgow, G. J., Melov, S., Newman, J. C., & Verdin, E. (2019) · Nature · doi:10.1038/s41586-019-1365-2 · Cited by 1,389
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
Cellular senescence promotes adverse effects of chemotherapy and cancer relapse
Demaria, M., O'Leary, M. N., Chang, J., Shao, L., Liu, S., Alimirah, F., Koenig, K., Le, C., Mitin, N., Deal, A. M., et al. (2017) · Cancer Discovery · doi:10.1158/2159-8290.cd-16-0241 · Cited by 1,338
Self-citationCytoplasmic chromatin triggers inflammation in senescence and cancer
Dou, Z., Ghosh, K., Vizioli, M. G., Zhu, J., Sen, P., Wangensteen, K. J., Simithy, J., Lan, Y., Lin, Y., Zhou, Z., et al. (2017) · Nature · doi:10.1038/nature24050 · Cited by 1,335
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
The twilight of immunity: emerging concepts in aging of the immune system
Nikolich-Žugich, J. (2018) · Nature Immunology · doi:10.1038/s41590-017-0006-x · Cited by 1,240
Mitochondrial Dysfunction Induces Senescence with a Distinct Secretory Phenotype
Wiley, C. D., Velarde, M. C., Lecot, P., Liu, S., Sarnoski, E. A., Freund, A., Shirakawa, K., Lim, H. W., Davis, S. S., Ramanathan, A., et al. (2016) · Cell Metabolism · doi:10.1016/j.cmet.2015.11.011 · Cited by 1,275
Self-citationSenescent cells: an emerging target for diseases of ageing
Childs, B. G., Gluscevic, M., Baker, D. J., Laberge, R.-M., Marquess, D., Dananberg, J., & van Deursen, J. M. (2017) · Nature Reviews Drug Discovery · doi:10.1038/nrd.2017.116 · Cited by 1,284
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
DNA damage and the balance between survival and death in cancer biology
Roos, W. P., Thomas, A. D., & Kaina, B. (2016) · Nature Reviews Cancer · doi:10.1038/nrc.2015.2 · Cited by 1,189
Mechanisms and functions of cellular senescence
Herranz, N., & Gil, J. (2018) · Journal of Clinical Investigation · doi:10.1172/jci95148 · Cited by 1,232
Recent Developments in Myofibroblast Biology
Hinz, B., Phan, S. H., Thannickal, V. J., Prunotto, M., Desmoulière, A., Varga, J., De Wever, O., Mareel, M., & Gabbiani, G. (2012) · The American Journal of Pathology · doi:10.1016/j.ajpath.2012.02.004 · Cited by 1,193
Senescence and the SASP: many therapeutic avenues
Birch, J., & Gil, J. (2020) · Genes & Development · doi:10.1101/gad.343129.120 · Cited by 1,177
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-citationForging a signature of in vivo senescence
Sharpless, N. E., & Sherr, C. J. (2015) · Nature Reviews Cancer · doi:10.1038/nrc3960 · Cited by 1,104
Cellular 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
Role of interleukin-6 in cancer progression and therapeutic resistance
Kumari, N., Dwarakanath, B. S. R., Das, A., & Bhatt, A. N. (2016) · Tumor Biology · doi:10.1007/s13277-016-5098-7 · Cited by 1,132
Lamin B1 loss is a senescence-associated biomarker
Freund, A., Laberge, R.-M., Demaria, M., & Campisi, J. (2012) · Molecular Biology of the Cell · doi:10.1091/mbc.e11-10-0884 · Cited by 1,046
Self-citationChien, Y., Scuoppo, C., Wang, X., Fang, X., Balgley, B., Bolden, J. E., Premsrirut, P., Luo, W., Chicas, A., Lee, C. S., et al. (2011) · Genes & Development · doi:10.1101/gad.17276711 · Cited by 1,046
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
Feedback between p21 and reactive oxygen production is necessary for cell senescence
Passos, J. F., Nelson, G., Wang, C., Richter, T., Simillion, C., Proctor, C. J., Miwa, S., Olijslagers, S., Hallinan, J., Wipat, A., et al. (2010) · Molecular Systems Biology · doi:10.1038/msb.2010.5 · Cited by 1,019
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-citationProgramming the magnitude and persistence of antibody responses with innate immunity
Kasturi, S. P., Skountzou, I., Albrecht, R. A., Koutsonanos, D., Tang, H., Nakaya, H. I., Ravindran, R., Stewart, S. M., Alam, M. S., Kwissa, M., et al. (2011) · Nature · doi:10.1038/nature09737 · Cited by 995
A Versatile Viral System for Expression and Depletion of Proteins in Mammalian Cells
Campeau, E., Ruhl, V. E., Rodier, F., Smith, C. L., Rahmberg, B. L., Fuss, J. O., Campisi, J., Yaswen, P., Cooper, P. K., & Kaufman, P. D. (2009) · PLoS ONE · doi:10.1371/journal.pone.0006529 · Cited by 962
Self-citationThe central role of DNA damage in the ageing process
Schumacher, B., Pothof, J., Vijg, J., & Hoeijmakers, J. H. J. (2021) · Nature · doi:10.1038/s41586-021-03307-7 · Cited by 907
Hewitt, G., Jurk, D., Marques, F. D. M., Correia-Melo, C., Hardy, T., Gackowska, A., Anderson, R., Taschuk, M., Mann, J., & Passos, J. F. (2012) · Nature Communications · doi:10.1038/ncomms1708 · Cited by 908
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
The senescence-associated secretory phenotype and its physiological and pathological implications
Wang, B., Han, J., Elisseeff, J. H., & Demaria, M. (2024) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-024-00727-x · Cited by 948
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
Chronic inflammation induces telomere dysfunction and accelerates ageing in mice
Jurk, D., Wilson, C., Passos, J. F., Oakley, F., Correia-Melo, C., Greaves, L., Saretzki, G., Fox, C., Lawless, C., Anderson, R., et al. (2014) · Nature Communications · doi:10.1038/ncomms5172 · Cited by 819
Mitochondria are required for pro-ageing features of the senescent phenotype
Correia‐Melo, C., Marques, F. D., Anderson, R., Hewitt, G., Hewitt, R., Cole, J., Carroll, B. M., Miwa, S., Birch, J., Merz, A., et al. (2016) · The EMBO Journal · doi:10.15252/embj.201592862 · Cited by 796
Senescence and cancer — role and therapeutic opportunities
Schmitt, C. A., Wang, B., & Demaria, M. (2022) · Nature Reviews Clinical Oncology · doi:10.1038/s41571-022-00668-4 · Cited by 794
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
Microenvironmental regulation of therapeutic response in cancer
Klemm, F., & Joyce, J. A. (2014) · Trends in Cell Biology · doi:10.1016/j.tcb.2014.11.006 · Cited by 795
Biomarkers, oxidative stress and autophagy in skin aging
Gu, Y., Han, J., Jiang, C., & Zhang, Y. (2020) · Ageing Research Reviews · doi:10.1016/j.arr.2020.101036 · Cited by 797
Telomere dysfunction in ageing and age-related diseases
Rossiello, F., Jurk, D., Passos, J. F., & d’Adda di Fagagna, F. (2022) · Nature Cell Biology · doi:10.1038/s41556-022-00842-x · Cited by 754
T cell anergy, exhaustion, senescence, and stemness in the tumor microenvironment
Crespo, J., Sun, H., Welling, T. H., Tian, Z., & Zou, W. (2013) · Current Opinion in Immunology · doi:10.1016/j.coi.2012.12.003 · Cited by 752
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
Identification of HSP90 inhibitors as a novel class of senolytics
Fuhrmann-Stroissnigg, H., Ling, Y. Y., Zhao, J., McGowan, S. J., Zhu, Y., Brooks, R. W., Grassi, D., Gregg, S. Q., Stripay, J. L., Dorronsoro, A., et al. (2017) · Nature Communications · doi:10.1038/s41467-017-00314-z · Cited by 701
Radiation-induced cell death mechanisms
Eriksson, D., & Stigbrand, T. I. (2010) · Tumor Biology · doi:10.1007/s13277-010-0042-8 · Cited by 704
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
Orjalo, A. V., Bhaumik, D., Gengler, B. K., Scott, G. K., & Campisi, J. (2009) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0905299106 · Cited by 654
Self-citationSenescent 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-citationTargeting cellular senescence with senotherapeutics: senolytics and senomorphics
Zhang, L. J., Pitcher, L. E., Prahalad, V., Niedernhofer, L. J., & Robbins, P. D. (2022) · FEBS Journal · doi:10.1111/febs.16350 · Cited by 674
Jurk, D., Wang, C., Miwa, S., Maddick, M., Korolchuk, V., Tsolou, A., Gonos, E. S., Thrasivoulou, C., Jill Saffrey, M., Cameron, K., et al. (2012) · Aging Cell · doi:10.1111/j.1474-9726.2012.00870.x · Cited by 598
The senescence-associated secretory phenotype and its regulation
Lopes-Paciencia, S., Saint-Germain, E., Rowell, M.-C., Ruiz, A. F., Kalegari, P., & Ferbeyre, G. (2019) · Cytokine · doi:10.1016/j.cyto.2019.01.013 · Cited by 601
Tau protein aggregation is associated with cellular senescence in the brain
Musi, N., Valentine, J. M., Sickora, K. R., Baeuerle, E., Thompson, C. S., Shen, Q., & Orr, M. E. (2018) · Aging Cell · doi:10.1111/acel.12840 · Cited by 595
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
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-citationRodier, F., Muñoz, D. P., Teachenor, R., Chu, V., Le, O., Bhaumik, D., Coppé, J.-P., Campeau, E., Beauséjour, C. M., Kim, S.-H., et al. (2011) · Journal of Cell Science · doi:10.1242/jcs.071340 · Cited by 535
Self-citationMechanisms underlying T cell ageing
Goronzy, J. J., & Weyand, C. M. (2019) · Nature Reviews Immunology · doi:10.1038/s41577-019-0180-1 · Cited by 506
Haigis, M. C., & Yankner, B. A. (2010) · Molecular Cell · doi:10.1016/j.molcel.2010.10.002 · Cited by 488
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-citationCancer and Inflammation: An Old Intuition with Rapidly Evolving New Concepts
Trinchieri, G. (2012) · Annual Review of Immunology · doi:10.1146/annurev-immunol-020711-075008 · Cited by 522
Immunosenescence: a key player in cancer development
Lian, J., Yue, Y., Yu, W., & Zhang, Y. (2020) · Journal of Hematology & Oncology · doi:10.1186/s13045-020-00986-z · Cited by 510
Bhaumik, D., Scott, G. K., Schokrpur, S., Patil, C. K., Orjalo, A. V., Rodier, F., Lithgow, G. J., & Campisi, J. (2009) · Aging · doi:10.18632/aging.100042 · Cited by 500
Self-citationCalder, P. C., Bosco, N., Bourdet‐Sicard, R., Capuron, L., Delzenne, N. M., Dore, J. M., Franceschi, C., Lehtinen, M. J., Recker, T., Salvioli, S., et al. (2017) · Ageing Research Reviews · doi:10.1016/j.arr.2017.09.001 · Cited by 524
Turinetto, V., Vitale, E., & Giachino, C. (2016) · International Journal of Molecular Sciences · doi:10.3390/ijms17071164 · Cited by 502
Ahmed, N., & Stenvers, K. L. (2013) · Frontiers in Oncology · doi:10.3389/fonc.2013.00256 · Cited by 492
Blocking PD-L1–PD-1 improves senescence surveillance and ageing phenotypes
Wang, T.-W., Johmura, Y., Suzuki, N., Omori, S., Migita, T., Yamaguchi, K., Hatakeyama, S., Yamazaki, S., Shimizu, E., Imoto, S., et al. (2022) · Nature · doi:10.1038/s41586-022-05388-4 · Cited by 469
Senescent Cells in Cancer Therapy: Friends or Foes?
Wang, B., Kohli, J., & Demaria, M. (2020) · Trends in Cancer · doi:10.1016/j.trecan.2020.05.004 · Cited by 508
Inflammation-induced DNA damage, mutations and cancer
Kay, J. E., Thadhani, E., Samson, L. D., & Engelward, B. P. (2019) · DNA repair · doi:10.1016/j.dnarep.2019.102673 · Cited by 495
The p53 network: cellular and systemic DNA damage responses in aging and Cancer
Reinhardt, H. C., & Schumacher, B. (2012) · Trends in Genetics · doi:10.1016/j.tig.2011.12.002 · Cited by 458
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
From Ancient Pathways to Aging Cells—Connecting Metabolism and Cellular Senescence
Wiley, C. D., & Campisi, J. (2016) · Cell Metabolism · doi:10.1016/j.cmet.2016.05.010 · Cited by 440
Self-citationCHK2 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
Inflammation and oncogenesis: a vicious connection
Grivennikov, S. I., & Karin, M. (2009) · Current Opinion in Genetics & Development · doi:10.1016/j.gde.2009.11.004 · Cited by 474
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-citationChronic inflammation and the hallmarks of aging
Baechle, J. J., Chen, N., Makhijani, P., Winer, S., Furman, D., & Winer, D. A. (2023) · Molecular Metabolism · doi:10.1016/j.molmet.2023.101755 · Cited by 471
Radiotherapy and the Tumor Stroma: The Importance of Dose and Fractionation
Hellevik, T., & Martínez-Zubiaurre, I. (2014) · Frontiers in Oncology · doi:10.3389/fonc.2014.00001 · Cited by 453
mTOR as a central regulator of lifespan and aging
Papadopoli, D. J., Boulay, K., Kazak, L., Pollak, M., Mallette, F. A., Topisirović, I., & Hulea, L. (2019) · F1000Research · doi:10.12688/f1000research.17196.1 · Cited by 447
Aging of the immune system: Focus on inflammation and vaccination
Pinti, M., Appay, V., Campisi, J., Frasca, D., Fülöp, T., Sauce, D., Larbi, A., Weinberger, B., & Cossarizza, A. (2016) · European Journal of Immunology · doi:10.1002/eji.201546178 · Cited by 439
Self-citationDNA Damage, DNA Repair, Aging, and NeurodegenerationPreprint
Maynard, S., Fang, E. F., Scheibye‐Knudsen, M., Croteau, D. L., & Bohr, V. A. (2015) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a025130 · Cited by 454
DNA Damage-Mediated Induction of a Chemoresistant Niche
Gilbert, L. A., & Hemann, M. T. (2010) · Cell · doi:10.1016/j.cell.2010.09.043 · Cited by 428
How vascular smooth muscle cell phenotype switching contributes to vascular disease
Cao, G., Xuan, X., Hu, J. H., Zhang, R., Jin, H., & Dong, H. (2022) · Cell Communication and Signaling · doi:10.1186/s12964-022-00993-2 · Cited by 472
Ortiz-Montero, P., Londoño-Vallejo, A., & Vernot, J.-P. (2017) · Cell Communication and Signaling · doi:10.1186/s12964-017-0172-3 · Cited by 428
Cellular senescence: a link between cancer and age-related degenerative disease?
Campisi, J., Andersen, J. K., Kapahi, P., & Melov, S. (2011) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2011.09.001 · Cited by 421
Self-citation
Metadata
- Authors
- Rodier, F., Coppé, J.-P., Patil, C. K., Hoeijmakers, W. A. M., Muñoz, D. P., Raza, S. R., Freund, A., Campeau, E., Davalos, A. R., & Campisi, J.
- Affiliations
- Lawrence Berkeley National Laboratory (US)
- Buck Institute for Research on Aging (US)
- Corresponding author
- Campisi, Judith
- Venue
- Nature Cell Biology
- Published
- 2009-07-13
- Volume
- 11
- Issue
- 8
- Pages
- 973-979
- ISSN
- 1465-7392 (ISSN-L)
- 1476-4679
- PMC
- PMC2743561
- OpenAlex
- W2116054786
- Cited by
- 2,232
- References
- 31
- Citations by year
- 2026: 126 · 2025: 143 · 2024: 152 · 2023: 158 · 2022: 159 · 2021: 168 · 2020: 154 · 2019: 147 · 2018: 139 · 2017: 149 · 2016: 113 · 2015: 105 · 2014: 118 · 2013: 102 · 2012: 108
- FWCI
- 64.86
- Type
- journal article
- Language
- en
- Update notices
- erratum (2009-10-01)
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (AG017242, P30AG025708, AG025708, P01AG017242)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- DNA damage response, senescence-associated secretory phenotype, IL-6 secretion, oncogene-induced senescence, ATM, NBS1, Chk2, DNA double-strand breaks, tumour invasiveness, senescence-associated inflammation, p53, retinoblastoma protein
- MeSH terms
- Cell Line, Cells, Cultured, DNA Damage, DNA-Binding Proteins, Enzyme-Linked Immunosorbent Assay, Fibroblasts, Humans, Male, Microscopy, Fluorescence, Nuclear Proteins, Transfection, Blotting, Western, Signal Transduction, Interleukin-6, Tumor Suppressor Protein p53, Cytokines, Telomere, Cellular Senescence, Protein Serine-Threonine Kinases, Cell Cycle Proteins, Telomerase, Cyclin-Dependent Kinase Inhibitor p16, Tumor Suppressor Proteins, RNA, Small Interfering, Green Fluorescent Proteins, Ataxia Telangiectasia Mutated Proteins, Checkpoint Kinase 2
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
