The Chromatin Landscape of Cellular Senescence

Criscione, Steven W.; Teo, Yee Voan; Neretti, Nicola

doi:10.1016/j.tig.2016.09.005

Cited by 137Telomeres, Telomerase, and SenescenceGenomics and Chromatin DynamicsGenetics, Aging, and Longevity in Model Organisms

The Chromatin Landscape of Cellular Senescence

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Criscione, Steven W., Teo, Yee Voan, Neretti, Nicola·2016·Trends in Genetics

DOI 10.1016/j.tig.2016.09.005PMC PMC5235059

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Abstract

Cellular senescence, an irreversible growth arrest triggered by a variety of stressors, plays important roles in normal physiology and tumor suppression, but accumulation of senescent cells with age contributes to the functional decline of tissues. Senescent cells undergo dramatic alterations to their chromatin landscape that affect genome accessibility and their transcriptional program. These include the loss of DNA-nuclear lamina interactions, the distension of centromeres, and changes in chromatin composition that can lead to the activation of retrotransposons. Here we discuss these findings, as well as recent advances in microscopy and genomics that have revealed the importance of the higher-order spatial organization of the genome in defining and maintaining the senescent state.

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Replicative senescence shows loss of long-range and gain of short-range interactions within chromosomes, implying that senescence-associated high-order chromatin interactions are stimulus and context dependent.
“Replicative senescence, on the other hand, showed loss of long-range and gain of short-range interactions within chromosomes (Criscione et al., 2016), implying that the nature of senescence-associated high-order chromatin interactions is stimulus and context dependent (Zirkel et al., 2018).”
From Cellular Senescence: Defining a Path Forward (2019) · cites this paper as Criscione et al., 2016
The Changes in chromosome organization section reports a genome-wide increase in short-range contacts in replicatively senescent cells. It does not report a corresponding loss of long-range within-chromosome interactions in those cells. The sentence attributes its broader stimulus-and-context inference to Zirkel et al., not to this source. (LLM, conf=0.85)
Experimental — accuracy not yet measured
LINE-1 elements fuel the SASP in addition to triggering genomic instability.
“Therefore, in addition to triggering genomic instability, these elements fuel the SASP (Criscione et al., 2016).”
From Cellular Senescence: Defining a Path Forward (2019) · cites this paper as Criscione et al., 2016
The section on chromatin structure says activated retrotransposons can propagate genomic instability through insertional mutagenesis. The Concluding remarks also link retrotransposition to new DNA damage, but attribute SASP gene activation to super-enhancer remodeling; they do not say LINE-1 elements fuel the SASP. Page numbers were not available in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measured
Pericentromeric regions are highly enriched for lamin-B1-positive regions in human fibroblasts, suggesting hSATII loci might be tethered to the nuclear membrane to prevent expansion and transcription.
“Pericentromeric regions are highly enriched for lamin-B1-positive regions in human fibroblasts (43), suggesting that the hSATII loci might be tethered to the nuclear membrane to prevent its expansion and transcription (44).”
From Chromatin conformational changes at human satellite II contribute to the senescence phenotype in the tumor microenvironment (2023) · cites this paper as [44]
The section on loss of DNA association with the nuclear envelope says the lamina interacts with heterochromatic domains and that loss of lamina components detaches those domains. The section on transcriptional changes says pericentric HSATII distends and becomes accessible in senescent cells. Neither passage establishes that pericentromeric regions are highly enriched for lamin-B1-positive regions in human fibroblasts or proposes that membrane tethering prevents HSATII expansion and transcription. (LLM, conf=0.78)
Experimental — accuracy not yet measured

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Sadaie, M., Salama, R., Carroll, T., Tomimatsu, K., Chandra, T., Young, A. R. J., Narita, M., Pérez-Mancera, P. A., Bennett, D. C., Chong, H., et al. (2013) · Genes & Development · doi:10.1101/gad.217281.113 · Cited by 323 · see citing works
Essential Requirement of BMPs-2/4 for Both Osteoblast and Osteoclast Formation in Murine Bone Marrow Cultures from Adult Mice: Antagonism by Noggin
Abe, E., Yamamoto, M., Taguchi, Y., Lecka‐Czernik, B., O’Brien, C. A., Economides, A. N., Stahl, N., Jilka, R. L., & Manolagas, S. C. (2000) · Journal of Bone and Mineral Research · doi:10.1359/jbmr.2000.15.4.663 · Cited by 319 · see citing works
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Senescence-Associated Secretory Phenotypes Reveal Cell-Nonautonomous Functions of Oncogenic RAS and the p53 Tumor Suppressor
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Transcriptional landscape of repetitive elements in normal and cancer human cells
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Bone Morphogenetic Protein-2 Stimulates Angiogenesis in Developing Tumors
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Global changes in the nuclear positioning of genes and intra- and interdomain genomic interactions that orchestrate B cell fate
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BMI1 Is Recruited to DNA Breaks and Contributes to DNA Damage-Induced H2A Ubiquitination and Repair
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Higher-order unfolding of satellite heterochromatin is a consistent and early event in cell senescence
Swanson, E. C., Manning, B., Zhang, H., & Lawrence, J. B. (2013) · Journal of Cell Biology · doi:10.1083/jcb.201306073 · Cited by 251 · cited 2× · see citing works
“It has been proposed that SADS formation is one of the early modifications to the chromatin landscape in senescence [63, 82], but whether it is required to induce or maintain the senescent state is still unclear.”
Background
Lamin B1 fluctuations have differential effects on cellular proliferation and senescence
Dreesen, O., Chojnowski, A., Ong, P. F., Zhao, T. Y., Common, J. E., Lunny, D., Lane, E. B., Lee, S. J., Vardy, L. A., Stewart, C. L., et al. (2013) · Journal of Cell Biology · doi:10.1083/jcb.201206121 · Cited by 250 · see citing works
HIF-1: A Target For Cancer, Ischemia and Inflammation—Too Good to be True?
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Loss of linker histone H1 in cellular senescence
Funayama, R., Saito, M., Tanobe, H., & Ishikawa, F. (2006) · The Journal of Cell Biology · doi:10.1083/jcb.200604005 · Cited by 241 · cited 2× · see citing works
“Indeed, SAHF, which have been shown to consist of a single chromosome [29, 33, 39], might represent an extreme case of chromosome shrinkage primarily driven by the condensation of heterochromatic LADs in the nuclear interior after they dissociate from the lamina.”
Background
Epigenetic Silencing of the p16 Tumor Suppressor Is Associated with Loss of CTCF Binding and a Chromatin Boundary
Witcher, M., & Emerson, B. M. (2009) · Molecular Cell · doi:10.1016/j.molcel.2009.04.001 · Cited by 235 · see citing works
Oncogene-induced telomere dysfunction enforces cellular senescence in human cancer precursor lesions.
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SIRT6 deacetylates H3K18ac at pericentric chromatin to prevent mitotic errors and cellular senescence
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Activation of DNA Damage Response Signaling by Condensed Chromatin
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Role of progerin-induced telomere dysfunction in HGPS premature cellular senescence
Benson, E. K., Lee, S. W., & Aaronson, S. A. (2010) · Journal of Cell Science · doi:10.1242/jcs.067306 · Cited by 185 · see citing works
Stable Cellular Senescence Is Associated with Persistent DDR Activation
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Telomere length in Hutchinson-Gilford Progeria Syndrome
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H2AX May Function as an Anchor to Hold Broken Chromosomal DNA Ends in Close Proximity
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Reorganization of chromosome architecture in replicative cellular senescence
Criscione, S. W., De Cecco, M., Siranosian, B., Zhang, Y., Kreiling, J. A., Sedivy, J. M., & Neretti, N. (2016) · Science Advances · doi:10.1126/sciadv.1500882 · Cited by 164 · see citing works
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Histone H3.3 and its proteolytically processed form drive a cellular senescence programme
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Derepression of <i>hTERT</i> gene expression promotes escape from oncogene-induced cellular senescence
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Bone morphogenetic protein 2 stimulation of tumor growth involves the activation of Smad-1/5
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Depletion of SIRT6 causes cellular senescence, DNA damage, and telomere dysfunction in human chondrocytes
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Several Distinct Polycomb Complexes Regulate and Co-Localize on the INK4a Tumor Suppressor Locus
Maertens, G. N., Messaoudi, S. E., Racek, T., Stock, J. K., Nicholls, J., Rodríguez‐Niedenführ, M., Gil, J., & Peters, G. G. (2009) · PLoS ONE · doi:10.1371/journal.pone.0006380 · Cited by 103 · see citing works
Mapping H4K20me3 onto the chromatin landscape of senescent cells indicates a function in control of cell senescence and tumor suppression through preservation of genetic and epigenetic stability
Nelson, D. M., Jaber‐Hijazi, F., Cole, J. J., Robertson, N., Pawlikowski, J. S., Norris, K., Criscione, S. W., Pchelintsev, N. A., Piscitello, D., Stong, N., et al. (2016) · Genome biology · doi:10.1186/s13059-016-1017-x · Cited by 103 · see citing works
Self-citation
Editorial
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Epigenetic Involvement in Hutchinson-Gilford Progeria Syndrome: A Mini-Review
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Replicative senescence is associated with nuclear reorganization and with DNA methylation at specific transcription factor binding sites
Hänzelmann, S., Beier, F., Gusmao, E. G., Koch, C., Hummel, S., Charapitsa, I., Joussen, S., Beneš, V., Brümmendorf, T. H., Reid, G., et al. (2015) · Clinical Epigenetics · doi:10.1186/s13148-015-0057-5 · Cited by 78 · see citing works
Activation of Bmp2-Smad1 Signal and Its Regulation by Coordinated Alteration of H3K27 Trimethylation in Ras-Induced Senescence
Kaneda, A., Fujita, T., Anai, M., Yamamoto, S., Nagae, G., Morikawa, M., Tsuji, S., Oshima, M., Miyazono, K., & Aburatani, H. (2011) · PLoS Genetics · doi:10.1371/journal.pgen.1002359 · Cited by 72 · see citing works
Autophagy-mediated degradation of nuclear envelope proteins during oncogene-induced senescence
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Old cells, new tricks: chromatin structure in senescence
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FOXA1 mediates p16INK4a activation during cellular senescence
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“Cellular senescence is a state of permanent growth arrest and, unsurprisingly, many of the genes that are downregulated during senescence are shared with the quiescent state and involve the cell-cycle pathway [64].”
Background
Quantitative assessment of higher‐order chromatin structure of the INK4/ARF locus in human senescent cells
Hirosue, A., Ishihara, K., Tokunaga, K., Watanabe, T., Saitoh, N., Nakamoto, M., Chandra, T., Narita, M., Shinohara, M., & Nakao, M. (2012) · Aging Cell · doi:10.1111/j.1474-9726.2012.00809.x · Cited by 44 · see citing works
Genome Reorganization During Aging of Dividing Cells
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Cellular Senescence: Defining a Path Forward
Gorgoulis, V., Adams, P. D., Alimonti, A., Bennett, D. C., Bischof, O., Bishop, C., Campisi, J., Collado, M., Evangelou, K., Ferbeyre, G., et al. (2019) · Cell · doi:10.1016/j.cell.2019.10.005 · Cited by 3,225 · see citing works
Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype
Kumari, R., & Jat, P. (2021) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2021.645593 · Cited by 1,622 · see citing works
Biomarkers of aging
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PML nuclear bodies and chromatin dynamics: catch me if you can!
Corpet, A., Kleijwegt, C., Roubille, S., Juillard, F., Jacquet, K., Texier, P., & Lomonte, P. (2020) · Nucleic Acids Research · doi:10.1093/nar/gkaa828 · Cited by 204 · see citing works
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 · see citing works
BiT age: A transcriptome‐based aging clock near the theoretical limit of accuracy
Meyer, D. H., & Schumacher, B. (2021) · Aging Cell · doi:10.1111/acel.13320 · Cited by 165 · see citing works
Notch Signaling Mediates Secondary Senescence
Teo, Y. V., Rattanavirotkul, N., Olova, N., Salzano, A., Quintanilla, A., Tarrats, N., Kiourtis, C., Müller, M., Green, A. R., Adams, P. D., et al. (2019) · Cell Reports · doi:10.1016/j.celrep.2019.03.104 · Cited by 149 · see citing works
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Cell‐free DNA as a biomarker of aging
Teo, Y. V., Capri, M., Morsiani, C., Pizza, G., Faria, A. M. C., Franceschi, C., & Neretti, N. (2018) · Aging Cell · doi:10.1111/acel.12890 · Cited by 152 · see citing works
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Senescence and the tumor-immune landscape: Implications for cancer immunotherapy
Chibaya, L., Snyder, J. T., & Ruscetti, M. A. (2022) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2022.02.005 · Cited by 138 · see citing works
MicroRNA Regulation of Oxidative Stress‐Induced Cellular Senescence
Bu, H., Wedel, S., Cavinato, M. S., & Jansen‐Dürr, P. (2017) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2017/2398696 · Cited by 123 · see citing works
A common signature of cellular senescence; does it exist?
Sikora, E., Bielak-Żmijewska, A., & Mosieniak, G. (2021) · Ageing Research Reviews · doi:10.1016/j.arr.2021.101458 · Cited by 120 · see citing works
NOTCH-mediated non-cell autonomous regulation of chromatin structure during senescence
Parry, A. J., Hoare, M., Bihary, D., Hänsel-Hertsch, R., Smith, S., Tomimatsu, K., Mannion, E., Smith, A., D’Santos, P., Russell, I. A., et al. (2018) · Nature Communications · doi:10.1038/s41467-018-04283-9 · Cited by 102 · see citing works
Cardiac cell senescence: molecular mechanisms, key proteins and therapeutic targets
Luan, Y., Zhu, X., Jiao, Y., Liu, H., Huang, Z., Pei, J., Xu, Y., Yang, Y., & Ren, K. (2024) · Cell Death Discovery · doi:10.1038/s41420-023-01792-5 · Cited by 106 · see citing works
The loss of heterochromatin is associated with multiscale three-dimensional genome reorganization and aberrant transcription during cellular senescencePreprint
Zhang, X., Liu, X., Du, Z., Wei, L., Fang, H., Dong, Q., Niu, J., Li, Y., Gao, J. T., Zhang, M. Q., et al. (2021) · Genome Research · doi:10.1101/gr.275235.121 · Cited by 100 · see citing works
The Nuclear Lamina as an Organizer of Chromosome Architecture
Shevelyov, Y. Y., & Ulianov, S. V. (2019) · Cells · doi:10.3390/cells8020136 · Cited by 97 · see citing works
Live imaging of chromatin distribution reveals novel principles of nuclear architecture and chromatin compartmentalization
Pavlov, D. A., Lorber, D., Bajpai, G., Reuveny, A., Roncato, F., Alon, R., Safran, S. A., & Volk, T. (2021) · Science Advances · doi:10.1126/sciadv.abf6251 · Cited by 99 · see citing works
Detect accessible chromatin using ATAC-sequencing, from principle to applications
Sun, Y., Miao, N., & Sun, T. (2019) · Hereditas · doi:10.1186/s41065-019-0105-9 · Cited by 93 · see citing works
The Histone Code of Senescence
Paluvai, H., Giorgio, E. D., & Brancolini, C. (2020) · Cells · doi:10.3390/cells9020466 · Cited by 94 · see citing works
Quadruplex Folding Promotes the Condensation of Linker Histones and DNAs via Liquid–Liquid Phase Separation
Mimura, M., Tomita, S., Shinkai, Y., Hosokai, T., Kumeta, H., Saio, T., Shiraki, K., & Kurita, R. (2021) · Journal of the American Chemical Society · doi:10.1021/jacs.1c03447 · Cited by 91 · see citing works
Nuclear Dynamics of Heterochromatin Repair
Amaral, N., Ryu, T., Li, X., & Chiolo, I. (2017) · Trends in Genetics · doi:10.1016/j.tig.2016.12.004 · Cited by 91 · see citing works
Cellular Senescence: The Trojan Horse in Chronic Lung Diseases
Hamsanathan, S., Alder, J. K., Sellarés, J., Rojas, M. M., Gurkar, A. U., & Mora, A. L. (2019) · American Journal of Respiratory Cell and Molecular Biology · doi:10.1165/rcmb.2018-0410tr · Cited by 87 · see citing works
Short-term gain, long-term pain: the senescence life cycle and cancer
Chan, A. S. L., & Narita, M. (2019) · Genes & Development · doi:10.1101/gad.320937.118 · Cited by 80 · see citing works
Chromatin Architectural Changes during Cellular Senescence and Aging
Sun, L., Yu, R., & Dang, W. (2018) · Genes · doi:10.3390/genes9040211 · Cited by 83 · see citing works
Forces driving the three‐dimensional folding of eukaryotic genomes
Rada-Iglesias, Á., Grosveld, F. G., & Papantonis, A. (2018) · Molecular Systems Biology · doi:10.15252/msb.20188214 · Cited by 81 · see citing works
Immune Aging and Immunotherapy in Cancer
Kaiser, M., Semeraro, M. D., Herrmann, M., Absenger, G., Gerger, A., & Renner, W. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22137016 · Cited by 78 · see citing works
Epigenomic drivers of immune dysfunction in aging
Keenan, C. R., & Allan, R. S. (2018) · Aging Cell · doi:10.1111/acel.12878 · Cited by 76 · see citing works
Lamina Associated Domains and Gene Regulation in Development and Cancer
Lochs, S. J. A., Kefalopoulou, S., & Kind, J. (2019) · Cells · doi:10.3390/cells8030271 · Cited by 74 · see citing works
The Regulatory Properties of the Ccr4–Not Complex
Hagkarim, N. C., & Grand, R. J. A. (2020) · Cells · doi:10.3390/cells9112379 · Cited by 70 · see citing works
The senescent cell epigenome
Yang, N., & Sen, P. (2018) · Aging · doi:10.18632/aging.101617 · Cited by 74 · see citing works
Senescence-activated enhancer landscape orchestrates the senescence-associated secretory phenotype in murine fibroblasts
Guan, Y., Zhang, C., Lyu, G., Zhang, X., Zhuang, T., Zhuang, T., Jia, L., Zhang, C., Zhang, C., Li, C., et al. (2020) · Nucleic Acids Research · doi:10.1093/nar/gkaa858 · Cited by 77 · see citing works
Epithelial cell senescence: an adaptive response to pre-carcinogenic stresses?
Abbadie, C., Pluquet, O., & Pourtier, A. (2017) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-017-2587-9 · Cited by 74 · see citing works
Oxidative Stress-Driven Cellular Senescence: Mechanistic Crosstalk and Therapeutic Horizons
Stojanović, B., Jovanovic, I., Stojanovic, M. D., Stojanović, B., Kovačević, V., Radosavljević, I., Jovanović, D., Kovačević, M. M., Zornić, N., Arsić, A. A., et al. (2025) · Antioxidants · doi:10.3390/antiox14080987 · Cited by 83 · see citing works
Role of Senescence and Aging in SARS-CoV-2 Infection and COVID-19 Disease
Lynch, S. M., Guo, G., Gibson, D. S., Bjourson, A. J., & Singh, T. (2021) · Cells · doi:10.3390/cells10123367 · Cited by 69 · see citing works
The response to DNA damage in heterochromatin domains
Fortuny, A., & Polo, S. E. (2018) · Chromosoma · doi:10.1007/s00412-018-0669-6 · Cited by 70 · see citing works
Senescent mesenchymal stem cells remodel extracellular matrix driving breast cancer cells to a more-invasive phenotype
Ghosh, D., Peña, C. M., Quach, N. D., Xuan, B., Lee, A. H., & Dawson, M. (2020) · Journal of Cell Science · doi:10.1242/jcs.232470 · Cited by 67 · see citing works
Aging of the Retina: Molecular and Metabolic Turbulences and Potential Interventions
Campello, L., Singh, N., Advani, J., Mondal, A. K., Corso‐Díaz, X., & Swaroop, A. (2021) · Annual Review of Vision Science · doi:10.1146/annurev-vision-100419-114940 · Cited by 67 · see citing works
“Bone-SASP” in Skeletal Aging
Fang, C., Liu, B., & Wan, M. (2023) · Calcified Tissue International · doi:10.1007/s00223-023-01100-4 · Cited by 69 · see citing works
Aberrant Function of the C-Terminal Tail of HIST1H1E Accelerates Cellular Senescence and Causes Premature Aging
Flex, E., Martinelli, S., Dijck, A. V., Ciolfi, A., Cecchetti, S., Coluzzi, E., Pannone, L., Andreoli, C., Radio, F. C., Pizzi, S., et al. (2019) · The American Journal of Human Genetics · doi:10.1016/j.ajhg.2019.07.007 · Cited by 58 · see citing works
Vascular Endothelial Senescence: Pathobiological Insights, Emerging Long Noncoding RNA Targets, Challenges and Therapeutic Opportunities
Sun, X., & Feinberg, M. W. (2021) · Frontiers in Physiology · doi:10.3389/fphys.2021.693067 · Cited by 55 · see citing works
Histone Variant H2A.J Marks Persistent DNA Damage and Triggers the Secretory Phenotype in Radiation-Induced Senescence
Isermann, A., Mann, C., & Rübe, C. E. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21239130 · Cited by 54 · see citing works
Dynamic 3D genome reorganization during senescence: defining cell states through chromatin
Shaban, H. A., & Gasser, S. M. (2023) · Cell Death and Differentiation · doi:10.1038/s41418-023-01197-y · Cited by 55 · see citing works
Cellular senescence-associated gene IFI16 promotes HMOX1-dependent evasion of ferroptosis and radioresistance in glioblastoma
Zhou, Y., Zeng, L., Cai, L., Wang, Z., Liu, X., Xiao, Y., Jin, X., Bai, Y., Lai, M., Li, H., et al. (2025) · Nature Communications · doi:10.1038/s41467-025-56456-y · Cited by 52 · see citing works
SAMMY-seq reveals early alteration of heterochromatin and deregulation of bivalent genes in Hutchinson-Gilford Progeria Syndrome
Sebestyén, E., Marullo, F., Lucini, F., Petrini, C., Bianchi, A., Valsoni, S., Olivieri, I., Antonelli, L., Gregoretti, F., Oliva, G., et al. (2020) · Nature Communications · doi:10.1038/s41467-020-20048-9 · Cited by 49 · see citing works
Form follows function: Nuclear morphology as a quantifiable predictor of cellular senescence
Belhadj, J., Surina, S., Hengstschläger, M., & Lomakin, A. J. (2023) · Aging Cell · doi:10.1111/acel.14012 · Cited by 48 · see citing works
The NSD2/WHSC1/MMSET methyltransferase prevents cellular senescence‐associated epigenomic remodeling
Tanaka, H., Igata, T., Etoh, K., Koga, T., Takebayashi, S., & Nakao, M. (2020) · Aging Cell · doi:10.1111/acel.13173 · Cited by 42 · see citing works
Cellular senescence in liver diseases: From molecular drivers to therapeutic targeting
Du, K., Umbaugh, D. S., Ren, N., & Diehl, A. M. (2025) · Journal of Hepatology · doi:10.1016/j.jhep.2025.08.021 · Cited by 42 · see citing works
Cannabidiol and Cannabigerol Inhibit Cholangiocarcinoma Growth In Vitro via Divergent Cell Death Pathways
Viereckl, M. J., Krutsinger, K., Apawu, A. K., Gu, J. H., Cardona, B., Barratt, D., & Han, Y. (2022) · Biomolecules · doi:10.3390/biom12060854 · Cited by 38 · see citing works
Cellular senescence as a response to multiwalled carbon nanotube (MWCNT) exposure in human mesothelial cells
Reamon-Buettner, S. M., Hackbarth, A., Leonhardt, A., Braun, A. C., & Ziemann, C. (2020) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2020.111412 · Cited by 36 · see citing works
The Genomic Health of Human Pluripotent Stem Cells: Genomic Instability and the Consequences on Nuclear Organization
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Authors: Criscione, S. W., Teo, Y. V., & Neretti, N.
Affiliations: Brown University (US)
Corresponding author: Neretti, Nicola
ORCID: Criscione, Steven W.
Teo, Yee Voan
Neretti, Nicola
Venue: Trends in Genetics
Publisher: Elsevier BV
Published: 2016-11
Volume: 32
Issue: 11
Pages: 751-761
ISSN: 0168-9525 (ISSN-L)
DOI: 10.1016/j.tig.2016.09.005
PMC: PMC5235059
OpenAlex: W2526226937
Cited by: 137
References: 104
Citations by year: 2026: 6 · 2025: 18 · 2024: 13 · 2023: 21 · 2022: 9 · 2021: 18 · 2020: 15 · 2019: 16 · 2018: 14 · 2017: 7
FWCI: 1.45
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Trends in Genetics (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institute on Aging (F31AG050365, R56AG050582)
National Institute of General Medical Sciences (T32GM007601, P20GM109035)
Topics: Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
Keywords: cellular senescence, chromatin landscape, retrotransposon activation, genome accessibility, transcriptional programs, 3D genome organization, senescence-associated heterochromatin foci, aging, tumor suppression
MeSH terms: Centromere, Chromatin, DNA, Heterochromatin, Histones, Humans, Transcription, Genetic, Cellular Senescence, Genomics, Nuclear Lamina

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The Chromatin Landscape of Cellular Senescence

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