The DOI matches its Crossref record; 37 of the 37 references it cites were found in a registry or an index.
Cytoplasmic chromatin triggers inflammation in senescence and cancer
Open accessAbstract
Chromatin is traditionally viewed as a nuclear entity that regulates gene expression and silencing. However, we recently discovered the presence of cytoplasmic chromatin fragments that pinch off from intact nuclei of primary cells during senescence, a form of terminal cell-cycle arrest associated with pro-inflammatory responses. The functional significance of chromatin in the cytoplasm is unclear. Here we show that cytoplasmic chromatin activates the innate immunity cytosolic DNA-sensing cGAS-STING (cyclic GMP-AMP synthase linked to stimulator of interferon genes) pathway, leading both to short-term inflammation to restrain activated oncogenes and to chronic inflammation that associates with tissue destruction and cancer. The cytoplasmic chromatin-cGAS-STING pathway promotes the senescence-associated secretory phenotype in primary human cells and in mice. Mice deficient in STING show impaired immuno-surveillance of oncogenic RAS and reduced tissue inflammation upon ionizing radiation. Furthermore, this pathway is activated in cancer cells, and correlates with pro-inflammatory gene expression in human cancers. Overall, our findings indicate that genomic DNA serves as a reservoir to initiate a pro-inflammatory pathway in the cytoplasm in senescence and cancer. Targeting the cytoplasmic chromatin-mediated pathway may hold promise in treating inflammation-related disorders.
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
“The DNA sensor cGAS and the adaptor protein STING have been reported to be major regulators of the SASP programme across species, presumably by activating NF-κB and the interferon response factor IRF3 (REFS60,112,113).”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · 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
“Cellular senescence is accompanied by substantial reorganization of the nuclear envelope and a breakdown in nucleocytoplasmic trafficking, including altered expression and degradation of Lamin B1, and the formation of cytoplasmic chromatin fragments (CCFs) [38–45].”
From Chemically induced reprogramming to reverse cellular aging (2023) · cites this paper as [39]
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 and others have previously described a role of the cGAS–STING pathway in the regulation of cellular senescence—a hallmark of ageing5–8.”
From cGAS–STING drives ageing-related inflammation and neurodegeneration (2023) · cites this paper as [7]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Loss of nuclear lamina can lead to the release of cytosolic chromatin fragments (CCFs) in the cytoplasm of senescent cells58–60”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [60]
The cited source says what the claim attributes to it.
In the citing paper
“Downregulation of Lamin B1 leads to collapse of the nuclear envelope, which can trigger release of chromatin fragments from the nucleus to the cytosol, termed cytoplasmic chromatin fragments (CCF).68”
From Cellular senescence and senescence-associated secretory phenotype via the cGAS-STING signaling pathway in cancer (2020) · cites this paper as [68]
The cited source says what the claim attributes to it.
In the citing paper
“However, Dou et al68 demonstrated that inhibiting the cGAS‐STING signaling pathway impaired the immuno‐surveillance of senescent hepatocytes and premalignant hepatocytes, resulting in tumorigenesis in the liver.”
From Cellular senescence and senescence-associated secretory phenotype via the cGAS-STING signaling pathway in cancer (2020) · cites this paper as [68]
The cited source says what the claim attributes to it.
In the citing paper
“The cGAS/STING pathway is considered a key regulator of SASP induction (Dou et al. 2017; Glück et al. 2017; Yang et al. 2017).”
From Senescence and the SASP: many therapeutic avenues (2020) · cites this paper as Dou et al. 2017
The cited source says what the claim attributes to it.
In the citing paper
“Previous research has revealed DNA damage products5–7 and retroelement amplification52 as upstream triggers of cGAS in senescence.”
From cGAS–STING drives ageing-related inflammation and neurodegeneration (2023) · cites this paper as [7]
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“Telomeric DNA damage is more senescence-specific and can be quantified by combining fluorescence in situ hybridization (FISH) for telomeric sequences and immunostaining (immunoFISH) for DSB-associated proteins22.”
From Guidelines for minimal information on cellular senescence experimentation in vivo (2024) · cites this paper as [22]
Experimental — accuracy not yet measuredIn the citing paper
“The mechanisms implicated in the accumulation of cytoplasmic DNA in senescent cells include compromised nuclear integrity due to loss of the nuclear lamina protein, Lamin B1 (Dou et al., 2017) and downregulation of cytoplasmic DNAases such as DNAase 2 and TREX1 (Takahashi et al., 2018) frequently observed in senescent cells.”
From Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021) · cites this paper as Dou et al., 2017
In the citing paper
“Recent studies have revealed that cytoplasmic chromatin fragments and transposable elements can stimulate cyclic GMP–AMP synthase linked to stimulator of interferon genes (cGAS-STING) pathway and regulate SASP both in vitro and in vivo where senescence was induced by different stimuli (Dou et al., 2017; Glück et al., 2017; Yang et al., 2017; Li and Chen, 2018).”
From Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021) · cites this paper as Dou et al., 2017
In the citing paper
“Loss of cGAS compromised senescence due to reduced SASP in different in vivo models and also accelerated the spontaneous immortalisation of mouse embryonic fibroblasts thereby highlighting the crucial role of the cGAS/STING pathway in tumor suppression due to immune-mediated clearance of premalignant cells (Dou et al., 2017; Glück et al., 2017; Umbreit and Pellman, 2017; Yang et al., 2017).”
From Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021) · cites this paper as Dou et al., 2017
In the citing paper
“Senescence-associated DNA damage is sensed via the cGAS–STING pathway, which activates the transcription factors interferon regulatory factor 3 (IRF3) and NF-κB, thereby inducing an interferon and SASP response55–58”
From COVID-19 and cellular senescence (2023) · cites this paper as [55]
In the citing paper
“Once CCF enter the cytoplasm, they are sensed by the cGAS-STING pathway (Dou et al., 2017; Gluck et al., 2017; Takahashi et al., 2018; Yang et al., 2017) (Fig. 2).”
From Cytoplasmic DNA: sources, sensing, and role in aging and disease (2021) · cites this paper as Dou et al., 2017
In the citing paper
“cGAS-STING activation leads to NF-κB activation of SASP genes downstream of STING instead of an interferon gene program, potentially due to p38-MAPK repression of interferon genes in senescent cells (Dou et al., 2017).”
From Cytoplasmic DNA: sources, sensing, and role in aging and disease (2021) · cites this paper as Dou et al., 2017
In the citing paper
“a phenotype which is thought to be partly dependent on p38-MAPK activation in senescent cells (Dou et al., 2017)”
From Cytoplasmic DNA: sources, sensing, and role in aging and disease (2021) · cites this paper as Dou et al., 2017
In the citing paper
“although MN-dependent cGAS activation of interferon genes is well documented in cancer cells”
From Cytoplasmic DNA: sources, sensing, and role in aging and disease (2021) · cites this paper as Dou et al., 2017
In the citing paper
“CCF activation of cGAS in senescent cells is typically associated with an NF-κB-dependent cytokine response”
From Cytoplasmic DNA: sources, sensing, and role in aging and disease (2021) · cites this paper as Dou et al., 2017
In the citing paper
“cGAS catalyzes the production of the second messenger cGMP that binds to stimulator of interferon genes (STING). This results in the phosphorylation of both interferon-regulatory factor 3 (IRF3) and of NF-κB transcription factors, thereby stimulating respectively the production of type I interferons and inflammatory cytokines [171,172,173,174].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [171]
In the citing paper
“The nuclear envelope of these micronuclei is unstable and can rupture, leading to the exposure of micronuclear DNA that induces a cellular immune response via cGAS [171,172,173].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [171]
In the citing paper
“Consistently, loss of cGAS and/or STING function reduces SASP factor levels in primary human cells and in mouse models of DNA damage-induced senescence [171,172,173].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [171]
In the citing paper
“Therefore, CCFs formation relies on the constitutive interaction between lamin B1 and LC3, and CCFs formation is required to reinforce OIS by initiating the SASP program [171,172].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [171]
In the citing paper
“Therefore, CCFs formation relies on the constitutive interaction between lamin B1 and LC3, and CCFs formation is required to reinforce OIS by initiating the SASP program [171,172].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [171]
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 Cancer Cell Line Encyclopedia enables predictive modelling of anticancer drug sensitivity
Barretina, J., Caponigro, G., Stransky, N., Venkatesan, K., Margolin, A. A., Kim, S., Wilson, C. J., Lehár, J., Kryukov, G. V., Sonkin, D., et al. (2012) · Nature · doi:10.1038/nature11003 · Cited by 7,950
Cyclic GMP-AMP Synthase Is a Cytosolic DNA Sensor That Activates the Type I Interferon Pathway
Sun, L., Wu, J., Du, F., Chen, X., & Chen, Z. J. (2013) · Science · doi:10.1126/science.1232458 · Cited by 4,996
STING is an endoplasmic reticulum adaptor that facilitates innate immune signalling
Ishikawa, H., & Barber, G. N. (2008) · Nature · doi:10.1038/nature07317 · Cited by 3,576
Self-citationAging, Cellular Senescence, and Cancer
Campisi, J. (2013) · Annual Review of Physiology · doi:10.1146/annurev-physiol-030212-183653 · Cited by 2,954 · cited 1×
“, Campisi, J. & Toussaint, O. Protocols to detect senescence-associated beta-galactosidase (SA-betagal) activity, a biomarker of senescent cells in culture and in vivo. Nat Protoc 4, 1798-1806, doi:10.1038/nprot.2009.191 nprot.2009.191 [pii] (2009). 32 Abe, T. et al. STING recognition of cytoplasmic DNA instigates cel…”
BackgroundInfluentialThe complex language of chromatin regulation during transcription
Berger, S. L. (2007) · Nature · doi:10.1038/nature05915 · Cited by 2,768
Self-citationSTING regulates intracellular DNA-mediated, type I interferon-dependent innate immunity
Ishikawa, H., Ma, Z., & Barber, G. N. (2009) · Nature · doi:10.1038/nature08476 · Cited by 2,759
Self-citationCyclic GMP-AMP Is an Endogenous Second Messenger in Innate Immune Signaling by Cytosolic DNA
Wu, J., Sun, L., Chen, X., Du, F., Shi, H., Chen, C., & Chen, Z. J. (2012) · Science · doi:10.1126/science.1229963 · Cited by 2,628
A complex secretory program orchestrated by the inflammasome controls paracrine senescence
Acosta, J. C., Banito, A., Wuestefeld, T., Georgilis, A., Janich, P., Morton, J. P., Athineos, D., Kang, T.-W., Lasitschka, F., Andrulis, M., et al. (2013) · Nature Cell Biology · doi:10.1038/ncb2784 · Cited by 2,278
Persistent DNA damage signalling triggers senescence-associated inflammatory cytokine secretion
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. (2009) · Nature Cell Biology · doi:10.1038/ncb1909 · Cited by 2,232
Debacq-Chainiaux, F., Erusalimsky, J. D., Campisi, J., & Toussaint, O. (2009) · Nature Protocols · doi:10.1038/nprot.2009.191 · Cited by 1,668
Cited by
Sorted by citations
Items 701–800 of 1,001
Antagonistic roles of cGAS/STING signaling in colorectal cancer chemotherapy
Liang, B., Xing, X., Storts, H., Ye, Z., Claybon, H., Austin, R., Ding, R., Liu, B., Wen, H., Miles, W. O., et al. (2024) · Frontiers in Oncology · doi:10.3389/fonc.2024.1441935 · Cited by 19
PSTK inhibition activates cGAS-STING, precipitating ferroptotic cell death in leukemic stem cells
He, L., Zhao, T., Leong, W. Z., Sharda, A., Mayerhofer, C., Mei, S., Bonilla, G. M., Menendez-Gonzalez, J. B., Gustafsson, K. M., Fukushima, T., et al. (2025) · Blood · doi:10.1182/blood.2024026040 · Cited by 19
Self-citationRIG-I-driven CDKN1A stabilization reinforces cellular senescence
Wang, C., Jiang, X., Li, H., Hu, J., Ji, Q., Wang, Q., Liu, X., Huang, D., Yan, K., Zhao, L., et al. (2025) · Science China Life Sciences · doi:10.1007/s11427-024-2844-8 · Cited by 19
The interplay between neutrophils and microbiota in cancer
Smith, C. K., & Trinchieri, G. (2018) · Journal of Leukocyte Biology · doi:10.1002/jlb.4ri0418-151r · Cited by 19
Perfluorocarbon Nanoemulsions for Combined Pulmonary siRNA Treatment of Lung Metastatic Osteosarcoma
Li, Z., Shen, Y., Wang, Y., Zhu, L., Zhu, C., Qian, C., Sun, M., & Oupický, D. (2019) · Advanced Therapeutics · doi:10.1002/adtp.201900039 · Cited by 19
How Cells Handle DNA Breaks during Mitosis: Detection, Signaling, Repair, and Fate Choice
Thompson, R. H., Gatenby, R., & Sidi, S. (2019) · Cells · doi:10.3390/cells8091049 · Cited by 19
Lambert, M., Leijonhufvud, C., Segerberg, F., Melenhorst, J. J., & Carlsten, M. (2020) · Methods in molecular biology · doi:10.1007/978-1-0716-0338-3_18 · Cited by 19
A Link between Replicative Stress, Lamin Proteins, and Inflammation
Willaume, S., Rass, E., Fontanilla-Ramirez, P., Moussa, A., Wanschoor, P., & Bertrand, P. (2021) · Genes · doi:10.3390/genes12040552 · Cited by 28
Targeting cellular senescence to combat cancer and ageing
Wang, C., Hao, X., & Zhang, R. (2022) · Molecular Oncology · doi:10.1002/1878-0261.13266 · Cited by 20
Research progress of the engagement of inorganic nanomaterials in cancer immunotherapy
Peng, T., Xu, T., & Liu, X. (2022) · Drug Delivery · doi:10.1080/10717544.2022.2086940 · Cited by 19
Stress-induced cellular senescence contributes to chronic inflammation and cancer progression.
KOBASHIGAWA, S., M. SAKAGUCHI, Y., MASUNAGA, S., & MORI, E. (2019) · Thermal Medicine · doi:10.3191/thermalmed.35.41 · Cited by 18
Senescence in cancer: Hallmarks, paradoxes, and therapeutic promise
Hinterleitner, C., Goldberg, H. V., McHugh, D., Barthet, V. J. A., Filliol, A. A., & Lowe, S. W. (2026) · Cell · doi:10.1016/j.cell.2026.03.005 · Cited by 20
cGAS-STING pathway in senescence-related inflammation
Chen, K., Liu, J., & Cao, X. (2017) · National Science Review · doi:10.1093/nsr/nwx146 · Cited by 18
Regulation of the Cell-Intrinsic DNA Damage Response by the Innate Immune Machinery
Hayman, T. J., & Glazer, P. M. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms222312761 · Cited by 19
STING‐mediated inflammation contributes to Gao binge ethanol feeding model
Wang, L., You, H., Meng, H., Pan, X., Chen, X., Bi, Y., Zhang, Y., Li, J., Yin, N., Zhang, Z., et al. (2021) · Journal of Cellular Physiology · doi:10.1002/jcp.30606 · Cited by 18
Kano, N., Ong, G. H., Ori, D., & Kawai, T. (2022) · Frontiers in Cellular and Infection Microbiology · doi:10.3389/fcimb.2022.910654 · Cited by 20
Potential role of cellular senescence in pulmonary arterial hypertension
Liu, L., Wei, Y., Giunta, S., He, Q., & Xia, S. (2022) · Clinical and Experimental Pharmacology and Physiology · doi:10.1111/1440-1681.13696 · Cited by 18
Chromosomal Instability as Enabling Feature and Central Hallmark of Breast Cancer
Castellanos, G., Valbuena, D. S., Pérez, E., Villegas, V. E., & Rondón‐Lagos, M. (2023) · Breast Cancer Targets and Therapy · doi:10.2147/bctt.s383759 · Cited by 22
cGLRs Join Their Cousins of Pattern Recognition Receptor Family to Regulate Immune Homeostasis
Kumar, V., & Stewart, J. H. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25031828 · Cited by 18
Patra, M., Klochendler, A., Condiotti, R., Kaffe, B., Elgavish, S., Drawshy, Z., Avrahami, D., Narita, M., Hofree, M., Drier, Y., et al. (2024) · Nucleic Acids Research · doi:10.1093/nar/gkae313 · Cited by 18
Liu, K., Zan, P., Li, Z., Lu, H., Liu, P., Zhang, L., Wang, H., Ma, X., Chen, F., Zhao, J., et al. (2024) · Advanced Healthcare Materials · doi:10.1002/adhm.202400623 · Cited by 20
Regulatory cellular and molecular networks in the bone microenvironment during aging
Zhang, L., Wang, Z., Zhang, Y., Ji, R., Li, Z., Zou, J., & Gao, B. (2024) · Life Medicine · doi:10.1093/lifemedi/lnae019 · Cited by 19
Huang, Y., Li, S., Ye, W., Wang, H., Su, J., Gao, L., Shi, R., Mou, X., Leng, S. X., Xiao, C., et al. (2025) · Vaccines · doi:10.3390/vaccines13040431 · Cited by 19
Genes and pathways involved in senescence bypass identified by functional genetic screens
Roupakia, E., Markopoulos, G. S., & Kolettas, E. (2021) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2021.111432 · Cited by 18
Sasaki, M., Sato, Y., & Nakanuma, Y. (2021) · Scientific Reports · doi:10.1038/s41598-021-91016-6 · Cited by 18
DNA methylation protects cancer cells against senescence
Chen, X., Yamaguchi, K., Rodgers, B., Goehrig, D., Vindrieux, D., Lahaye, X., Nolot, M., Ferry, L., Lanciano, S., Martin, N., et al. (2025) · Nature Communications · doi:10.1038/s41467-025-61157-7 · Cited by 17
Targeting cGAS-STING signaling and cell death modes in cancer and autoimmune diseases
Zhou, J., Yang, Y., Fang, Y., Du, X., Ying, Z., & Rao, C. (2025) · Cytokine & Growth Factor Reviews · doi:10.1016/j.cytogfr.2025.07.004 · Cited by 18
Jayaraman, S., Eswaran, A., Rajagopal, P., Palanisamy, C. P., Veerakumar, P., Veeraraghavan, V. P., & Sirasanagandla, S. R. (2026) · Biogerontology · doi:10.1007/s10522-026-10402-7 · Cited by 17
cGAS-STING Pathway as the Target of Immunotherapy for Lung Cancer
Ge, H., Dan, Q., & Yang, Y. (2022) · Current Cancer Drug Targets · doi:10.2174/1568009623666221115095114 · Cited by 17
Cao, N., Wang, Z., Huang, C., Chen, B., Zhao, P., Xu, Y., & Tian, Y. (2023) · Archives of Gerontology and Geriatrics · doi:10.1016/j.archger.2023.105080 · Cited by 18
Proteogenomic characterization of skull-base chordoma
Zhang, Q., Xu, Z., Han, R., Wang, Y., Ye, Z., Zhu, J., Cai, Y., Zhang, F., Zhao, J., Yao, B., et al. (2024) · Nature Communications · doi:10.1038/s41467-024-52285-7 · Cited by 17
Self-citationDiscovery of Turn-On Fluorescent Probes for Detecting Bcl-2 Protein
Liu, T., Dong, G., Xu, F., Han, B., Fang, H., Huang, Y. H., Zhou, Y., Du, L., & Li, M. (2019) · Analytical Chemistry · doi:10.1021/acs.analchem.8b05853 · Cited by 17
SPANX Control of Lamin A/C Modulates Nuclear Architecture and Promotes Melanoma Growth
Lazar, I., Fabre, B., Feng, Y., Khateb, A., Turko, P., Gómez, J. M. M., Frederick, D. T., Levesque, M. P., Feld, L., Zhang, G., et al. (2020) · Molecular Cancer Research · doi:10.1158/1541-7786.mcr-20-0291 · Cited by 17
Nucleic Acid-Induced Signaling in Chronic Viral Liver Disease
Suarez, A. A. R., Testoni, B., Baumert, T. F., & Lupberger, J. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2020.624034 · Cited by 18
Sivananthan, A., Shields, D. S., Fisher, R., Hou, W., Zhang, X., Franicola, D., Epperly, M. W., Wipf, P., & Greenberger, J. S. (2018) · Radiation Research · doi:10.1667/rr15199.1 · Cited by 17
Molecular pathobiology of scleritis and its therapeutic implications
Das, U. N. (2019) · International Journal of Ophthalmology · doi:10.18240/ijo.2020.01.23 · Cited by 17
Cytosolic DNA crosstalk in senescence: a new axis of inflammatory signaling?
Dou, Z., Kreiling, J. A., Heynen‐Genel, S., Jurk, D., Neretti, N., Adams, P. D., Sedivy, J. M., & Passos, J. F. (2025) · The EMBO Journal · doi:10.1038/s44318-025-00531-z · Cited by 17
Self-citationRegulation of cancer by inflammasomes: from inflammation to tumorigenesis
Malvankar, S., Jaiswal, P., Bhat, P. P., & Mehto, S. (2025) · Frontiers in Immunology · doi:10.3389/fimmu.2025.1611719 · Cited by 16
Organelle-specific signaling of cGAS–STING
Liu, S., Wang, A., Chen, C., & Xu, P. (2025) · Trends in Cell Biology · doi:10.1016/j.tcb.2025.08.007 · Cited by 16
STING-mediated neuroinflammation: a therapeutic target in neurodegenerative diseases
Zhang, H., He, Z., Yin, C., Yang, S., Li, J., Lin, H. R., Hu, G., Wu, A., Qin, D., Yu, L., et al. (2025) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2025.1659216 · Cited by 16
Chronic inflammation evoked by pathogenic stimulus during carcinogenesis
Brücher, B. L. D. M., & Jamall, I. S. (2019) · 4open · doi:10.1051/fopen/2018006 · Cited by 16
Dhillon, V. S., Deo, P., Bonassi, S., & Fenech, M. F. (2021) · Mutation Research/Reviews in Mutation Research · doi:10.1016/j.mrrev.2021.108372 · Cited by 16
The Nuclear Envelope as a Regulator of Immune Cell Function
Selezneva, A. I., Gibb, A. J., & Willis, D. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.840069 · Cited by 16
Wu, S. K., Ariffin, J. K., Tay, S. C., & Picone, R. (2023) · Aging Cell · doi:10.1111/acel.13766 · Cited by 17
Ursino, C., Mouric, C., Gros, L., Bonnefoy, N., & Faget, J. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1170321 · Cited by 17
Potential cGAS-STING pathway functions in DNA damage responses, DNA replication and DNA repair
Zierhut, C. (2023) · DNA repair · doi:10.1016/j.dnarep.2023.103608 · Cited by 17
The molecular mechanism of dsDNA sensing through the cGAS-STING pathway
Shinde, O., & Li, P. (2024) · Advances in immunology · doi:10.1016/bs.ai.2024.02.003 · Cited by 16
Chen, J., Li, G., He, X., Chen, Z., Chen, Z., Liu, D., Guo, S., Huang, T., Lan, P., Lan, P., et al. (2023) · Gastroenterology report · doi:10.1093/gastro/goae045 · Cited by 16
Guduric‐Fuchs, J., Pedrini, E., Bertelli, P. M., McDonnell, S., Pathak, V., McLoughlin, K. J., O’Neill, C. L., Stitt, A. W., & Medina, R. J. (2024) · Aging Cell · doi:10.1111/acel.14240 · Cited by 17
Ding, H., Zhang, Q., Yang, R., Fu, L., Jiang, H., Zhu, Q., & Tai, S. (2024) · iScience · doi:10.1016/j.isci.2024.111594 · Cited by 17
Expanding the Role of STING in Cellular Homeostasis and Transformation
Li, J., & Bakhoum, S. F. W. (2019) · Trends in cancer · doi:10.1016/j.trecan.2019.02.001 · Cited by 16
Wang, D.-H., He, X. J., & He, Q. (2019) · Bioscience Reports · doi:10.1042/bsr20190459 · Cited by 16
Chen, Y., Zhu, S., Fu, S., Li, Z., Huang, F., Yin, H., & Chen, Z. (2019) · Journal of Innovative Optical Health Sciences · doi:10.1142/s1793545820500029 · Cited by 16
MYSM1 Suppresses Cellular Senescence and the Aging Process to Prolong Lifespan
Tian, M., Huang, Y., Song, Y., Li, W., Zhao, P., Liu, W., Wu, K., & Wu, J. (2020) · Advanced Science · doi:10.1002/advs.202001950 · Cited by 16
Purification of micronuclei from cultured cells by flow cytometry
Toufektchan, E., & Maciejowski, J. (2021) · STAR Protocols · doi:10.1016/j.xpro.2021.100378 · Cited by 18
Liang, L., Shen, Y., Hu, Y., Liu, H., & Cao, J. (2022) · PLoS Pathogens · doi:10.1371/journal.ppat.1010233 · Cited by 16
Zhang, N., Shang, M., Li, H., Wu, L., Dong, M., Huang, B., Lü, J., & Zhang, Y. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23073911 · Cited by 17
Feunteun, J., Ostyn, P., & Delaloge, S. (2022) · iScience · doi:10.1016/j.isci.2022.104217 · Cited by 16
Cellular Senescence and Ageing
Reed, R., & Miwa, S. (2023) · Sub-cellular biochemistry/Subcellular biochemistry · doi:10.1007/978-3-031-21410-3_7 · Cited by 16
Digital Inference of Immune Microenvironment Reveals Low-Risk Subtype of Early Lung Adenocarcinoma
Kurbatov, V., Balayev, A., Saffarzadeh, A. G., Heller, D. R., Boffa, D. J., Blasberg, J. D., Lü, J., & Khan, S. A. (2019) · The Annals of Thoracic Surgery · doi:10.1016/j.athoracsur.2019.08.050 · Cited by 16
Deciphering the role of skin aging in pigmentary disorders
Yang, Y., Wu, Y., Xiang, L. F., Picardo, M., & Zhang, C. (2024) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2024.12.032 · Cited by 17
Cao, Z., Zhang, Y. X., Jia, H., Sun, X., Feng, Y., Wu, H., Xu, B., & Wei, Z. (2025) · Cytokine · doi:10.1016/j.cyto.2025.156873 · Cited by 16
Cai, T., Liang, Z., Chen, Z., Li, Y., Xiao, W., Liang, W., Xie, H., Liu, H., Zeng, Z., Yang, X., et al. (2025) · Autophagy · doi:10.1080/15548627.2025.2551680 · Cited by 15
Alipour-Khezri, E., Moqadami, A., Vahed, S. Z., & Barzegari, A. (2025) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2025.118790 · Cited by 17
cGAS–STING signaling pathway as a therapeutic target in human diseases
Xiao, Y., Ma, Y., Zhao, J., Zhang, X., Gan, C., Gao, J., & Huang, Z. (2025) · Chinese Medical Journal · doi:10.1097/cm9.0000000000003904 · Cited by 15
Cellular senescence as a source of SARS‐CoV‐2 quasispecies
Karakasiliοtis, I., Lаgopati, N., Evangelou, K., & Gorgoulis, V. G. (2021) · FEBS Journal · doi:10.1111/febs.16230 · Cited by 15
Suzuki, K., Imaoka, T., Tomita, M., Sasatani, M., Doi, K., Tanaka, S., Kai, M., Yamada, Y., & Kakinuma, S. (2023) · Journal of Radiation Research · doi:10.1093/jrr/rrad003 · Cited by 16
Cytosolic DNA sensors and glial responses to endogenous DNA
Suptela, A. J., & Marriott, I. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1130172 · Cited by 15
Aging and oral squamous cell carcinoma development: the role of cellular senescence
Niklander, S. E., Aránguiz, P., Faunes, F., & Flores, R. (2023) · Frontiers in Oral Health · doi:10.3389/froh.2023.1285276 · Cited by 17
Dormancy of cutaneous melanoma
Singvogel, K., & Schittek, B. (2024) · Cancer Cell International · doi:10.1186/s12935-024-03278-5 · Cited by 15
Wu, Y., Li, Y., Yan, N., Huang, J., Li, X., Zhang, K., Lu, Z., Qiu, Z., & Cheng, H. B. (2024) · Journal of Controlled Release · doi:10.1016/j.jconrel.2024.04.008 · Cited by 15
Shafqat, A., Masters, M. C., Tripathi, U., Tchkonia, T., Kirkland, J. L., & Hashmi, S. K. (2024) · Ageing Research Reviews · doi:10.1016/j.arr.2024.102400 · Cited by 15
Manganese boosts natural killer cell function via cGAS–STING mediated UTX expression
Ming, Q., Liu, J., Lv, Z., Wang, T., Fan, R., Zhang, Y., Chen, M., Sun, Y., Han, W., & Mei, Q. (2024) · MedComm · doi:10.1002/mco2.683 · Cited by 15
Recent insights into the causes and consequences of chromosome mis-segregation
Devillers, R., dos Santos, A., Destombes, Q., Laplante, M., & Elowe, S. (2024) · Oncogene · doi:10.1038/s41388-024-03163-5 · Cited by 18
Soh, L.-J., Lee, S.-Y., Roebuck, M. M., & Wong, P. (2024) · Life Sciences · doi:10.1016/j.lfs.2024.123112 · Cited by 15
Autophagy-dependent splicing control directs translation toward inflammation during senescence
Kim, J., Lee, Y., Jeon, T., Ju, S., Kim, J., Kim, M.-S., & Kang, C. (2024) · Developmental Cell · doi:10.1016/j.devcel.2024.10.008 · Cited by 19
Bypassing Border Control: Nuclear Envelope Rupture in Disease
Houthaeve, G., Robijns, J., Braeckmans, K., & Vos, W. H. D. (2017) · Physiology · doi:10.1152/physiol.00029.2017 · Cited by 16
Combining Radiation Therapy With Interferons: Back to the Future
Goedegebuure, R. S. A., Vonk, C. M., Kooij, L. P., Derks, S., & Thijssen, V. L. (2020) · International Journal of Radiation Oncology*Biology*Physics · doi:10.1016/j.ijrobp.2020.02.016 · Cited by 16
Nakamura, N. (2021) · International Journal of Radiation Biology · doi:10.1080/09553002.2021.1955998 · Cited by 15
Physical Forces and Transient Nuclear Envelope Rupture during Metastasis: The Key for Success?
Gauthier, B. R., Lorenzo, P. I., & Comaills, V. (2021) · Cancers · doi:10.3390/cancers14010083 · Cited by 15
The multifaceted role of micronuclei in tumour progression: A whole organism perspective.
Guscott, M. A., Saha, A., Maharaj, J., & McClelland, S. E. (2022) · The International Journal of Biochemistry & Cell Biology · doi:10.1016/j.biocel.2022.106300 · Cited by 16
Pruthi, D. K., Miller, G., Ankerst, D. P., Neumair, M., Umberto Capitanio, A., Correa, A. F., Lane, B. R., Roussel, E., McGregor, T. B., Derweesh, I., et al. (2023) · The Journal of Urology · doi:10.1097/ju.0000000000003650 · Cited by 15
Neuroinflammation and Disease: Pathways and Opportunities
Hoffman, O., Varvel, N. H., Roopra, A., & Dingledine, R. J. (2025) · The Annual Review of Pharmacology and Toxicology · doi:10.1146/annurev-pharmtox-062124-043519 · Cited by 14
Mitotic SENP3 activation couples with cGAS signaling in tumor cells to stimulate anti-tumor immunity
Hu, G., Chen, Y., Yang, X., Wang, Y., He, J., Wang, T., Fan, Q., Deng, L., Tu, J., Tan, H., et al. (2022) · Cell Death and Disease · doi:10.1038/s41419-022-05063-6 · Cited by 14
The Potent and Paradoxical Biology of Cellular Senescence in Cancer
Romesser, P. B., & Lowe, S. W. (2023) · Annual Review of Cancer Biology · doi:10.1146/annurev-cancerbio-061421-124434 · Cited by 15
Senescence and Immunotherapy: Redundant Immunomodulatory Pathways Promote Resistance
Oesterreich, S., & Aird, K. M. (2023) · Cancer Immunology Research · doi:10.1158/2326-6066.cir-23-0051 · Cited by 14
Radiation-Induced Innate Neutrophil Response in Tumor Is Mediated by the CXCLs/CXCR2 Axis
Zhang, F., Mulvaney, O., Salcedo, E., Manna, S., Zhu, J. Z., Wang, T., Ahn, C. W., Pop, L. M., & Hannan, R. (2023) · Cancers · doi:10.3390/cancers15235686 · Cited by 15
Self-citationXu, M., Xia, Z.-Y., Sun, J., Liu, C., An, Y., Xu, J., Zhang, S.-H., Zhong, X., Zeng, N., Ma, S., et al. (2024) · Frontiers in Immunology · doi:10.3389/fimmu.2024.1395047 · Cited by 14
Self-citationD’Ordine, A. M., Jogl, G., & Sedivy, J. M. (2024) · Nature Communications · doi:10.1038/s41467-024-48066-x · Cited by 15
Uncoupling of mTORC1 from E2F activity maintains DNA damage and senescence
Daigh, L. H., Saha, D., Rosenthal, D. L., Ferrick, K. R., & Meyer, T. (2024) · Nature Communications · doi:10.1038/s41467-024-52820-6 · Cited by 16
Combined external beam radiotherapy with carbon ions and tumor targeting endoradiotherapy
Melzig, C., Golestaneh, A. F., Mier, W., Schwager, C., Das, S., Schlegel, J., Lasitschka, F., Kauczor, H., Debus, J., Haberkorn, U., et al. (2018) · Oncotarget · doi:10.18632/oncotarget.25695 · Cited by 14
Cytokine Storm as a Cellular Response to dsDNA Breaks: A New Proposal
Shabrish, S., & Mittra, I. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.622738 · Cited by 14
Epigenetic Dysregulation Induces Translocation of Histone H3 into Cytoplasm
Wang, Z., Chen, J., Gao, C., Xiao, Q., Wang, X., Tang, S., Li, Q., Zhong, B., Song, Z., Shu, H., et al. (2021) · Advanced Science · doi:10.1002/advs.202100779 · Cited by 14
Chen, J., Chen, X., Li, T., Wang, L., & Lin, G. (2022) · International Immunopharmacology · doi:10.1016/j.intimp.2022.108866 · Cited by 14
Bordoni, V., Mariotti, D., Matusali, G., Colavita, F., Cimini, E., Ippolito, G., & Agrati, C. (2022) · Cells · doi:10.3390/cells11182912 · Cited by 14
Yoshioka, K., Matsuno, Y., Hyodo, M., & Fujimori, H. (2019) · Cancers · doi:10.3390/cancers11111643 · Cited by 14
Biologically based models of cancer risk in radiation research
Kaiser, J. C., Blettner, M., & Stathopoulos, G. T. (2020) · International Journal of Radiation Biology · doi:10.1080/09553002.2020.1784490 · Cited by 14
Pan, Y., Gu, Z., Lyu, Y., Yang, Y., Chung, M., Pan, X., & Cai, S. (2022) · Rejuvenation Research · doi:10.1089/rej.2022.0021 · Cited by 15
Snowbarger, J. M., Koganti, P., & Spruck, C. (2024) · Biomolecules · doi:10.3390/biom14101250 · Cited by 14
Genome instability and crosstalk with the immune response
Chabanon, R. M., Danlos, F. X., Ouali, K., & Postel-Vinay, S. C. (2025) · Genome Medicine · doi:10.1186/s13073-025-01509-6 · Cited by 16
Metadata
- Authors
- Dou, Z., Ghosh, K., Vizioli, M. G., Zhu, J., Sen, P., Wangensteen, K. J., Simithy, J., Lan, Y., Lin, Y., Zhou, Z., Capell, B. C., Xu, C., Xu, M., Kieckhaefer, J. E., Jiang, T., Shoshkes-Carmel, M., Tanim, K. M. A. A., Barber, G. N., Seykora, J. T., Millar, S. E., Kaestner, K. H., Garcia, B. A., Adams, P. D., & Berger, S. L.
- Affiliations
- University of Pennsylvania (US)
- Cancer Research UK Scotland Institute (GB)
- Peking University (CN)
- Abramson Cancer Center (US)
- University of Miami (US)
- Sanford Burnham Prebys Medical Discovery Institute (US)
- Corresponding author
- Adams, Peter D.
- Berger, Shelley L.
- ORCID
- Venue
- Nature
- Published
- 2017-10
- Volume
- 550
- Issue
- 7676
- Pages
- 402-406
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC5850938
- OpenAlex
- W2762611634
- Cited by
- 1,335
- References
- 37
- Citations by year
- 2026: 177 · 2025: 157 · 2024: 184 · 2023: 156 · 2022: 174 · 2021: 158 · 2020: 127 · 2019: 115 · 2018: 75 · 2017: 10
- FWCI
- 40.47
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- ENLIGHTEN (Jurnal Bimbingan dan Konseling Islam) (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- National Institutes of Health (CA078831)
- National Institute on Aging (K99AG053406, P01AG031862)
- National Cancer Institute (P01CA196539, R01CA078831)
- National Institute of Allergy and Infectious Diseases (R01AI079336)
- National Institute of Diabetes and Digestive and Kidney Diseases (K08DK106478)
- National Institute of Environmental Health Sciences (P30ES013508)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (K08AR070289, P30AR069589, T32AR007465)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- cGAS-STING pathway, cytosolic DNA sensing, cellular senescence, senescence-associated secretory phenotype, chronic inflammation, tumor surveillance, oncogenic Ras, ionizing radiation, innate immunity, tumor inflammation
- MeSH terms
- STING Protein, Cyclic Guanosine Monophosphate-Adenosine Monophosphate Synthase, Animals, Chromatin, Cytoplasm, Female, Humans, Immunity, Innate, Inflammation, Liver, Male, Membrane Proteins, Neoplasms, Nucleotidyltransferases, Radiation, Ionizing, Oncogene Protein p21(ras), Cytokines, Cellular Senescence, Cell Line, Tumor, Mice
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
