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Cell biology

The beginning of the end

Nature volume 505, pages 35–36 (2014)Cite this article

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A Correction to this article was published on 08 January 2014

Studies in mice and humans suggest that cellular senescence, the cessation of cell proliferation that is known to suppress cancer and promote ageing, may have evolved to regulate embryonic development.

Cells that experience certain types of stress, particularly stress that is potentially cancer-causing, undergo an essentially permanent arrest of proliferation termed cellular senescence1. Since its formal description in the 1960s, cellular senescence has been thought both to suppress the development of cancer and to promote ageing. Support for these roles has come from tumour studies in mice and humans2, and from the realization that senescent cells secrete proteins that cause inflammation, a hallmark of ageing tissues3. More recently, a complex inflammatory response called the senescence-associated secretory phenotype (SASP) was shown to facilitate tissue repair and remodelling, and to help the immune system recognize and eventually remove senescent cells4. These multiple functions of cellular senescence are not mutually exclusive, but they raise an interesting teleological question: for what purpose did senescence evolve? Findings by Muñoz-Espín et al.5 and Storer et al.6, published in Cell, suggest a surprising answer: to fine-tune embryogenesis.

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Figure 1: Senescence modules.

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  1. Judith Campisi is at the Buck Institute for Research on Aging, Novato, California 94945, USA, and at the Lawrence Berkeley National Laboratory, Berkeley, California.,

    Judith Campisi

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  1. Judith Campisi
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Correspondence to Judith Campisi.

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Campisi, J. The beginning of the end. Nature 505, 35–36 (2014). https://doi.org/10.1038/nature12844

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