Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

The role of senescent cells in ageing

Subjects

Abstract

Cellular senescence has historically been viewed as an irreversible cell-cycle arrest mechanism that acts to protect against cancer, but recent discoveries have extended its known role to complex biological processes such as development, tissue repair, ageing and age-related disorders. New insights indicate that, unlike a static endpoint, senescence represents a series of progressive and phenotypically diverse cellular states acquired after the initial growth arrest. A deeper understanding of the molecular mechanisms underlying the multi-step progression of senescence and the development and function of acute versus chronic senescent cells may lead to new therapeutic strategies for age-related pathologies and extend healthy lifespan.

This is a preview of subscription content, access via your institution

Access options

Rent or buy this article

Prices vary by article type

from$1.95

to$39.95

Prices may be subject to local taxes which are calculated during checkout

Figure 1: Senescence-inducing stimuli and main effector pathways.
Figure 2: Hypothetical multi-step senescence model.
Figure 3: Acute and chronic senescent cells.
Figure 4: Mechanisms of tissue and organ deterioration by cellular senescence.

References

  1. Campisi, J. Aging, cellular senescence, and cancer. Annu. Rev. Physiol. 75, 685–705 (2013)

    CAS  PubMed  Google Scholar 

  2. Kuilman, T., Michaloglou, C., Mooi, W. J. & Peeper, D. S. The essence of senescence. Genes Dev. 24, 2463–2479 (2010)

    CAS  PubMed  PubMed Central  Google Scholar 

  3. López-Otin, C., Blasco, M. A., Partridge, L., Serrano, M. & Kroemer, G. The hallmarks of aging. Cell 153, 1194–1217 (2013)

    PubMed  PubMed Central  Google Scholar 

  4. Adams, P. D. Healing and hurting: molecular mechanisms, functions, and pathologies of cellular senescence. Mol. Cell 36, 2–14 (2009)

    CAS  PubMed  Google Scholar 

  5. Newgard, C. B. & Sharpless, N. E. Coming of age: molecular drivers of aging and therapeutic opportunities. J. Clin. Invest. 123, 946–950 (2013)

    CAS  PubMed  PubMed Central  Google Scholar 

  6. Tchkonia, T., Zhu, Y., van Deursen, J., Campisi, J. & Kirkland, J. L. Cellular senescence and the senescent secretory phenotype: therapeutic opportunities. J. Clin. Invest. 123, 966–972 (2013)

    CAS  PubMed  PubMed Central  Google Scholar 

  7. Hayflick, L. & Moorhead, P. S. The serial cultivation of human diploid cell strains. Exp. Cell Res. 25, 585–621 (1961)A pioneering study that introduced the term senescence to describe the phenomenon of permanent growth arrest of primary human cells after extensive serial passaging in culture.

    CAS  PubMed  Google Scholar 

  8. Bodnar, A. G. et al. Extension of life-span by introduction of telomerase into normal human cells. Science 279, 349–352 (1998)

    ADS  CAS  PubMed  Google Scholar 

  9. Serrano, M., Lin, A. W., McCurrach, M. E., Beach, D. & Lowe, S. W. Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a. Cell 88, 593–602 (1997)The study that established the concept of oncogene-induced senescence.

    CAS  PubMed  Google Scholar 

  10. Rajagopalan, S. & Long, E. O. Cellular senescence induced by CD158d reprograms natural killer cells to promote vascular remodeling. Proc. Natl Acad. Sci. USA 109, 20596–20601 (2012)

    ADS  CAS  PubMed  PubMed Central  Google Scholar 

  11. Muñoz-Espin, D. et al. Programmed cell senescence during mammalian embryonic development. Cell 155, 1104–1118 (2013)

    PubMed  Google Scholar 

  12. Storer, M. et al. Senescence is a developmental mechanism that contributes to embryonic growth and patterning. Cell 155, 1119–1130 (2013)References 10, 11, 12 are studies demonstrating that senescence has a central role in tissue remodelling during embryogenesis.

    CAS  PubMed  Google Scholar 

  13. Jun, J. I. & Lau, L. F. The matricellular protein CCN1 induces fibroblast senescence and restricts fibrosis in cutaneous wound healing. Nature Cell Biol. 12, 676–685 (2010)

    CAS  PubMed  Google Scholar 

  14. Krizhanovsky, V. et al. Senescence of activated stellate cells limits liver fibrosis. Cell 134, 657–667 (2008)References 14, 15 show that senescent cells that are produced after tissue damage act to curb fibrosis.

    CAS  PubMed  PubMed Central  Google Scholar 

  15. Baker, D. J. et al. Opposing roles for p16Ink4a and p19Arf in senescence and ageing caused by BubR1 insufficiency. Nature Cell Biol. 10, 825–836 (2008); corrigendum. 14, 649 (2012)A study that demonstrated a causal link between cellular senescence and age-related tissue deterioration, and the concept of assisted cycling.

    CAS  PubMed  Google Scholar 

  16. Baker, D. J. et al. Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders. Nature 479, 232–236 (2011)A study showing that clearance of p16Ink4a-positive senescent cells can delay age-related degenerative pathologies in a progeroid mouse model.

    ADS  CAS  PubMed  PubMed Central  Google Scholar 

  17. Nardella, C., Clohessy, J. G., Alimonti, A. & Pandolfi, P. P. Pro-senescence therapy for cancer treatment. Nature Rev. Cancer 11, 503–511 (2011)

    CAS  Google Scholar 

  18. Sedelnikova, O. A. et al. Senescing human cells and ageing mice accumulate DNA lesions with unrepairable double-strand breaks. Nature Cell Biol. 6, 168–170 (2004)

    CAS  PubMed  Google Scholar 

  19. von Zglinicki, T. Oxidative stress shortens telomeres. Trends Biochem. Sci. 27, 339–344 (2002)

    CAS  PubMed  Google Scholar 

  20. Aird, K. M. et al. Suppression of nucleotide metabolism underlies the establishment and maintenance of oncogene-induced senescence. Cell Rep. 3, 1252–1265 (2013)

    CAS  PubMed  Google Scholar 

  21. Di Micco, R. et al. Oncogene-induced senescence is a DNA damage response triggered by DNA hyper-replication. Nature 444, 638–642 (2006)

    ADS  CAS  PubMed  Google Scholar 

  22. Lazzerini Denchi, E., Attwooll, C., Pasini, D. & Helin, K. Deregulated E2F activity induces hyperplasia and senescence-like features in the mouse pituitary gland. Mol. Cell. Biol. 25, 2660–2672 (2005)

    PubMed  Google Scholar 

  23. Kaplon, J. et al. A key role for mitochondrial gatekeeper pyruvate dehydrogenase in oncogene-induced senescence. Nature 498, 109–112 (2013)

    ADS  CAS  PubMed  Google Scholar 

  24. Kondoh, H. et al. Glycolytic enzymes can modulate cellular life span. Cancer Res. 65, 177–185 (2005)

    CAS  PubMed  Google Scholar 

  25. Dörr, J. R. et al. Synthetic lethal metabolic targeting of cellular senescence in cancer therapy. Nature 501, 421–425 (2013)References 20, 23, 25 revealed that metabolic mechanisms are causally implicated in the induction and maintenance of the senescent state.

    ADS  PubMed  Google Scholar 

  26. Shamma, A. et al. Rb Regulates DNA damage response and cellular senescence through E2F-dependent suppression of N-ras isoprenylation. Cancer Cell 15, 255–269 (2009)

    CAS  PubMed  Google Scholar 

  27. Ben-Porath, I. & Weinberg, R. A. The signals and pathways activating cellular senescence. Int. J. Biochem. Cell Biol. 37, 961–976 (2005)

    CAS  PubMed  Google Scholar 

  28. Moiseeva, O., Mallette, F. A., Mukhopadhyay, U. K., Moores, A. & Ferbeyre, G. DNA damage signaling and p53-dependent senescence after prolonged beta-interferon stimulation. Mol. Biol. Cell 17, 1583–1592 (2006)

    CAS  PubMed  PubMed Central  Google Scholar 

  29. Romanov, V. S. et al. p21(Waf1) is required for cellular senescence but not for cell cycle arrest induced by the HDAC inhibitor sodium butyrate. Cell Cycle 9, 3945–3955 (2010)

    CAS  PubMed  Google Scholar 

  30. Lapak, K. M. & Burd, C. E. The molecular balancing act of p16INK4a in cancer and aging. Mol. Cancer Res. 167–183 (2014)

  31. Hein, N. et al. in Senescence (ed. Nagata, T. ) Ch. 9,. 171–208 (2012)

  32. Baker, D. J. et al. BubR1 insufficiency causes early onset of aging-associated phenotypes and infertility in mice. Nature Genet. 36, 744–749 (2004)

    CAS  PubMed  Google Scholar 

  33. Schmidt, S. et al. The centrosome and mitotic spindle apparatus in cancer and senescence. Cell Cycle 9, 4469–4473 (2010)

    CAS  PubMed  Google Scholar 

  34. Freund, A., Patil, C. K. & Campisi, J. p38MAPK is a novel DNA damage response-independent regulator of the senescence-associated secretory phenotype. EMBO J. 30, 1536–1548 (2011)

    CAS  PubMed  PubMed Central  Google Scholar 

  35. Passos, J. F. et al. Feedback between p21 and reactive oxygen production is necessary for cell senescence. Mol. Syst. Biol. 6, 347 (2010)

    PubMed  PubMed Central  Google Scholar 

  36. Baker, D. J., Weaver, R. L. & van Deursen, J. M. p21 both attenuates and drives senescence and aging in BubR1 progeroid mice. Cell Rep. 3, 1164–1174 (2013)

    CAS  PubMed  PubMed Central  Google Scholar 

  37. Grove, G. L. & Cristofalo, V. J. Characterization of the cell cycle of cultured human diploid cells: effects of aging and hydrocortisone. J. Cell. Physiol. 90, 415–422 (1977)

    CAS  PubMed  Google Scholar 

  38. Choudhury, A. R. et al. Cdkn1a deletion improves stem cell function and lifespan of mice with dysfunctional telomeres without accelerating cancer formation. Nature Genet. 39, 99–105 (2007)

    CAS  PubMed  Google Scholar 

  39. Siegel, J. J. & Amon, A. New insights into the troubles of aneuploidy. Annu. Rev. Cell Dev. Biol. 28, 189–214 (2012)

    CAS  PubMed  PubMed Central  Google Scholar 

  40. Vredeveld, L. C. et al. Abrogation of BRAFV600E-induced senescence by PI3K pathway activation contributes to melanomagenesis. Genes Dev. 26, 1055–1069 (2012)

    CAS  PubMed  PubMed Central  Google Scholar 

  41. Lapasset, L. et al. Rejuvenating senescent and centenarian human cells by reprogramming through the pluripotent state. Genes Dev. 25, 2248–2253 (2011)

    CAS  PubMed  PubMed Central  Google Scholar 

  42. De Cecco, M. et al. Genomes of replicatively senescent cells undergo global epigenetic changes leading to gene silencing and activation of transposable elements. Aging Cell 12, 247–256 (2013)

    CAS  PubMed  Google Scholar 

  43. Wang, J. et al. Inhibition of activated pericentromeric SINE/Alu repeat transcription in senescent human adult stem cells reinstates self-renewal. Cell Cycle 10, 3016–3030 (2011)

    CAS  PubMed  PubMed Central  Google Scholar 

  44. Ivanov, A. et al. Lysosome-mediated processing of chromatin in senescence. J. Cell Biol. 202, 129–143 (2013)

    CAS  PubMed  PubMed Central  Google Scholar 

  45. Purvis, J. E. et al. p53 dynamics control cell fate. Science 336, 1440–1444 (2012)

    ADS  CAS  PubMed  PubMed Central  Google Scholar 

  46. Freund, A., Laberge, R. M., Demaria, M. & Campisi, J. Lamin B1 loss is a senescence-associated biomarker. Mol. Biol. Cell 23, 2066–2075 (2012)

    CAS  PubMed  PubMed Central  Google Scholar 

  47. Shimi, T. et al. The role of nuclear lamin B1 in cell proliferation and senescence. Genes Dev. 25, 2579–2593 (2011)

    CAS  PubMed  PubMed Central  Google Scholar 

  48. Shah, P. P. et al. Lamin B1 depletion in senescent cells triggers large-scale changes in gene expression and the chromatin landscape. Genes Dev. 27, 1787–1799 (2013)

    CAS  PubMed  PubMed Central  Google Scholar 

  49. Funayama, R., Saito, M., Tanobe, H. & Ishikawa, F. Loss of linker histone H1 in cellular senescence. J. Cell Biol. 175, 869–880 (2006)

    CAS  PubMed  PubMed Central  Google Scholar 

  50. Narita, M. et al. A novel role for high-mobility group a proteins in cellular senescence and heterochromatin formation. Cell 126, 503–514 (2006)

    CAS  PubMed  Google Scholar 

  51. Zhang, R., Chen, W. & Adams, P. D. Molecular dissection of formation of senescence-associated heterochromatin foci. Mol. Cell. Biol. 27, 2343–2358 (2007)

    CAS  PubMed  PubMed Central  Google Scholar 

  52. Swanson, E. C., Manning, B., Zhang, H. & Lawrence, J. B. Higher-order unfolding of satellite heterochromatin is a consistent and early event in cell senescence. J. Cell Biol. 929–942 (2013)

  53. Shelton, D. N., Chang, E., Whittier, P. S., Choi, D. & Funk, W. D. Microarray analysis of replicative senescence. Curr. Biol. 9, 939–945 (1999)

    CAS  PubMed  Google Scholar 

  54. Zhang, H., Pan, K. H. & Cohen, S. N. Senescence-specific gene expression fingerprints reveal cell-type-dependent physical clustering of up-regulated chromosomal loci. Proc. Natl Acad. Sci. USA 100, 3251–3256 (2003)

    ADS  CAS  PubMed  PubMed Central  Google Scholar 

  55. Coppé, J. P. et al. Senescence-associated secretory phenotypes reveal cell-nonautonomous functions of oncogenic RAS and the p53 tumor suppressor. PLoS Biol. 6, e301 (2008)

    PubMed Central  Google Scholar 

  56. Rodier, F. et al. Persistent DNA damage signalling triggers senescence-associated inflammatory cytokine secretion. Nature Cell Biol. 11, 973–979 (2009); erratum. 11, 1272 (2009)

    CAS  PubMed  Google Scholar 

  57. Kuilman, T. & Peeper, D. S. Senescence-messaging secretome: SMS-ing cellular stress. Nature Rev. Cancer 9, 81–94 (2009)

    CAS  Google Scholar 

  58. Coppé, J. P. et al. Tumor suppressor and aging biomarker p16INK4a induces cellular senescence without the associated inflammatory secretory phenotype. J. Biol. Chem. 286, 36396–36403 (2011)

    PubMed  PubMed Central  Google Scholar 

  59. Coppé, J. P., Kauser, K., Campisi, J. & Beausejour, C. M. Secretion of vascular endothelial growth factor by primary human fibroblasts at senescence. J. Biol. Chem. 281, 29568–29574 (2006)

    PubMed  Google Scholar 

  60. Freund, A., Orjalo, A. V., Desprez, P. Y. & Campisi, J. Inflammatory networks during cellular senescence: causes and consequences. Trends Mol. Med. 16, 238–246 (2010)

    CAS  PubMed  PubMed Central  Google Scholar 

  61. Laberge, R. M., Awad, P., Campisi, J. & Desprez, P. Y. Epithelial-mesenchymal transition induced by senescent fibroblasts. Cancer Microenviron. 5, 39–44 (2012)

    CAS  PubMed  Google Scholar 

  62. Binet, R. et al. WNT16B is a new marker of cellular senescence that regulates p53 activity and the phosphoinositide 3-kinase/AKT pathway. Cancer Res. 69, 9183–9191 (2009)

    CAS  PubMed  PubMed Central  Google Scholar 

  63. Kuilman, T. et al. Oncogene-induced senescence relayed by an interleukin-dependent inflammatory network. Cell 133, 1019–1031 (2008)

    CAS  PubMed  Google Scholar 

  64. Yang, G. et al. The chemokine growth-regulated oncogene 1 (Gro-1) links RAS signaling to the senescence of stromal fibroblasts and ovarian tumorigenesis. Proc. Natl Acad. Sci. USA 103, 16472–16477 (2006)

    ADS  CAS  PubMed  PubMed Central  Google Scholar 

  65. Benz, G., Holzel, D. & Schmoeckel, C. Inflammatory cellular infiltrates in melanocytic nevi. Am. J. Dermatopathol. 13, 538–542 (1991)

    CAS  PubMed  Google Scholar 

  66. Finkel, T., Serrano, M. & Blasco, M. A. The common biology of cancer and ageing. Nature 448, 767–774 (2007)

    ADS  CAS  PubMed  Google Scholar 

  67. Matheu, A. et al. Delayed ageing through damage protection by the Arf/p53 pathway. Nature 448, 375–379 (2007)

    ADS  CAS  PubMed  Google Scholar 

  68. Baker, D. J. et al. Increased expression of BubR1 protects against aneuploidy and cancer and extends healthy lifespan. Nature Cell Biol. 15, 96–102 (2013)

    CAS  PubMed  Google Scholar 

  69. Jun, J. I. & Lau, L. F. Cellular senescence controls fibrosis in wound healing. Aging 2, 627–631 (2010)

    CAS  PubMed  PubMed Central  Google Scholar 

  70. Wang, J., Geiger, H. & Rudolph, K. L. Immunoaging induced by hematopoietic stem cell aging. Curr. Opin. Immunol. 23, 532–536 (2011)

    CAS  PubMed  Google Scholar 

  71. Nikolich-Žugich, J. Ageing and life-long maintenance of T-cell subsets in the face of latent persistent infections. Nature Rev. Immunol. 8, 512–522 (2008)

    Google Scholar 

  72. Roninson, I. B. Tumor cell senescence in cancer treatment. Cancer Res. 63, 2705–2715 (2003)

    CAS  PubMed  Google Scholar 

  73. Le, O. N. et al. Ionizing radiation-induced long-term expression of senescence markers in mice is independent of p53 and immune status. Aging Cell 9, 398–409 (2010)

    CAS  PubMed  Google Scholar 

  74. Allan, J. M. & Travis, L. B. Mechanisms of therapy-related carcinogenesis. Nature Rev. Cancer 5, 943–955 (2005)

    CAS  PubMed  Google Scholar 

  75. Jurk, D. et al. Postmitotic neurons develop a p21-dependent senescence-like phenotype driven by a DNA damage response. Aging Cell 11, 996–1004 (2012)A study showing that post-mitotic cells can obtain several key characteristics of senescent cells.

    CAS  PubMed  Google Scholar 

  76. Minamino, T. et al. A crucial role for adipose tissue p53 in the regulation of insulin resistance. Nature Med. 15, 1082–1087 (2009)

    CAS  PubMed  Google Scholar 

  77. Herbig, U., Ferreira, M., Condel, L., Carey, D. & Sedivy, J. M. Cellular senescence in aging primates. Science 311, 1257 (2006)

    CAS  PubMed  Google Scholar 

  78. Lawless, C. et al. Quantitative assessment of markers for cell senescence. Exp. Gerontol. 45, 772–778 (2010)

    CAS  PubMed  Google Scholar 

  79. Wang, C. et al. DNA damage response and cellular senescence in tissues of aging mice. Aging Cell 8, 311–323 (2009)

    CAS  PubMed  Google Scholar 

  80. Krishnamurthy, J. et al. p16INK4a induces an age-dependent decline in islet regenerative potential. Nature 443, 453–457 (2006)

    ADS  CAS  PubMed  Google Scholar 

  81. Jeyapalan, J. C., Ferreira, M., Sedivy, J. M. & Herbig, U. Accumulation of senescent cells in mitotic tissue of aging primates. Mech. Ageing Dev. 128, 36–44 (2007)

    CAS  PubMed  Google Scholar 

  82. Naylor, R. M., Baker, D. J. & van Deursen, J. M. Senescent cells: a novel therapeutic target for aging and age-related diseases. Clin. Pharmacol. Ther. 93, 105–116 (2013)

    CAS  PubMed  Google Scholar 

  83. Sherr, C. J. The Pezcoller lecture: cancer cell cycles revisited. Cancer Res. 60, 3689–3695 (2000)

    CAS  PubMed  Google Scholar 

  84. Campisi, J. Cellular senescence: putting the paradoxes in perspective. Curr. Opin. Genet. Dev. 21, 107–112 (2011)

    CAS  PubMed  Google Scholar 

  85. Coppé, J. P., Desprez, P. Y., Krtolica, A. & Campisi, J. The senescence-associated secretory phenotype: the dark side of tumor suppression. Annu. Rev. Pathol. 5, 99–118 (2010)

    PubMed  PubMed Central  Google Scholar 

  86. Rodier, F. & Campisi, J. Four faces of cellular senescence. J. Cell Biol. 192, 547–556 (2011)

    CAS  PubMed  PubMed Central  Google Scholar 

  87. Brack, A. S. et al. Increased Wnt signaling during aging alters muscle stem cell fate and increases fibrosis. Science 317, 807–810 (2007)

    ADS  CAS  PubMed  Google Scholar 

  88. Krtolica, A. et al. GROα regulates human embryonic stem cell self-renewal or adoption of a neuronal fate. Differentiation 81, 222–232 (2011)

    CAS  PubMed  PubMed Central  Google Scholar 

  89. Pricola, K. L., Kuhn, N. Z., Haleem-Smith, H., Song, Y. & Tuan, R. S. Interleukin-6 maintains bone marrow-derived mesenchymal stem cell stemness by an ERK1/2-dependent mechanism. J. Cell. Biochem. 108, 577–588 (2009)

    CAS  PubMed  PubMed Central  Google Scholar 

  90. Conboy, I. M. et al. Rejuvenation of aged progenitor cells by exposure to a young systemic environment. Nature 433, 760–764 (2005)

    ADS  CAS  PubMed  Google Scholar 

  91. Parrinello, S., Coppe, J. P., Krtolica, A. & Campisi, J. Stromal–epithelial interactions in aging and cancer: senescent fibroblasts alter epithelial cell differentiation. J. Cell Sci. 118, 485–496 (2005)

    CAS  PubMed  Google Scholar 

  92. Acosta, J. C. et al. A complex secretory program orchestrated by the inflammasome controls paracrine senescence. Nature Cell Biol. 15, 978–990 (2013)

    CAS  PubMed  Google Scholar 

  93. Nelson, G. et al. A senescent cell bystander effect: senescence-induced senescence. Aging Cell 11, 345–349 (2012)References 92, 94 show that senescent cells can induce senescence in neighbouring cells through paracrine mechanisms.

    CAS  PubMed  Google Scholar 

  94. Faggioli, F., Wang, T., Vijg, J. & Montagna, C. Chromosome-specific accumulation of aneuploidy in the aging mouse brain. Hum. Mol. Genet. 21, 5246–5253 (2012)

    CAS  PubMed  PubMed Central  Google Scholar 

  95. Garinis, G. A., van der Horst, G. T., Vijg, J. & Hoeijmakers, J. H. DNA damage and ageing: new-age ideas for an age-old problem. Nature Cell Biol. 10, 1241–1247 (2008)

    CAS  PubMed  Google Scholar 

  96. Xue, W. et al. Senescence and tumour clearance is triggered by p53 restoration in murine liver carcinomas. Nature 445, 656–660 (2007)

    CAS  PubMed  PubMed Central  Google Scholar 

  97. Kang, T. W. et al. Senescence surveillance of pre-malignant hepatocytes limits liver cancer development. Nature 479, 547–551 (2011)

    ADS  CAS  PubMed  Google Scholar 

  98. Krishnamurthy, J. et al. Ink4a/Arf expression is a biomarker of aging. J. Clin. Invest. 114, 1299–1307 (2004)

    CAS  PubMed  PubMed Central  Google Scholar 

  99. Bhaumik, D. et al. MicroRNAs miR-146a/b negatively modulate the senescence-associated inflammatory mediators IL-6 and IL-8. Aging 1, 402–411 (2009)

    CAS  PubMed  PubMed Central  Google Scholar 

Download references

Acknowledgements

I thank J. Campisi, J. Kirkland, R. Naylor, B. Childs, D. Baker, R. Urrutia, M. McNiven and R. Bram for helpful discussions and comments on the manuscript. I apologize to those whom I was unable to reference owing to space limitations. This work was supported by grants from the Paul Glenn Foundation and the National Institutes of Health (R01CA96985, R01CA166347 and AG41122-01P2).

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Jan M. van Deursen.

Ethics declarations

Competing interests

The author declares no competing financial interests.

PowerPoint slides

Rights and permissions

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

van Deursen, J. The role of senescent cells in ageing. Nature 509, 439–446 (2014). https://doi.org/10.1038/nature13193

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1038/nature13193

This article is cited by

Comments

By submitting a comment you agree to abide by our Terms and Community Guidelines. If you find something abusive or that does not comply with our terms or guidelines please flag it as inappropriate.

Search

Quick links

Nature Briefing

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing