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Killing the old: cell senescence in atherosclerosis

Nature Reviews Cardiology volume 14, pages 89 (2017) | Download Citation

  • An Erratum to this article was published on 12 January 2017

This article has been updated

Atherosclerosis is a disease of ageing, and the most common cause of death in the industrialized world. Cell senescence and the therapeutic removal of senescent cells using 'senolytics' are topical areas of science and translational medicine. A new study reports surprising findings on cell senescence and atherosclerosis with important therapeutic implications.

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  • 12 January 2017

    In the version of this article initially published online and in print, the red symbol in Figure 1 should be IL-1α, and not IL-1β. The error has been corrected for the HTML and PDF versions of the article.


  1. 1.

    et al. Senescent intimal foam cells are deleterious at all stages of atherosclerosis. Science 354, 472–477 (2016).

  2. 2.

    et al. Vascular smooth muscle cells undergo telomere-based senescence in human atherosclerosis: effects of telomerase and oxidative stress. Circ. Res. 99, 156–164 (2006).

  3. 3.

    , , & Senescent vascular smooth muscle cells drive inflammation through an interleukin-1α-dependent senescence-associated secretory phenotype. Arterioscler. Thromb. Vasc. Biol. 35, 1963–1974 (2015).

  4. 4.

    et al. Aging of mice is associated with p16Ink4a- and β-galactosidase- positive macrophage accumulation that can be induced in young mice by senescent cells. Aging (Albany NY) 8, 1294–1315 (2016).

  5. 5.

    & Ageing: out with the old. Nature 530, 164–165 (2016).

  6. 6.

    et al. Expression of Chr9p21 genes CDKN2B (p15INK4b), CDKN2A (p16INK4a, 14ARF) and MTAP in human atherosclerotic plaque. Atherosclerosis 214, 264–270 (2011).

  7. 7.

    et al. Downregulation of the tumour suppressor p16INK4A contributes to the polarisation of human macrophages toward an adipose tissue macrophage (ATM)-like phenotype. Diabetologia 54, 3150–3156 (2011).

  8. 8.

    et al. p16INK4a deficiency promotes IL-4-induced polarization and inhibits proinflammatory signaling in macrophages. Blood 118, 2556–2566 (2011).

  9. 9.

    et al. Chronic senolytic treatment alleviates established vasomotor dysfunction in aged or atherosclerotic mice. Aging Cell 15, 973–977 (2016).

  10. 10.

    et al. Monocyte/macrophage suppression in CD11b diphtheria toxin receptor transgenic mice differentially affects atherogenesis and established plaques. Circ. Res. 100, 884–893 (2007).

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This work was funded by British Heart Foundation Grants RG/13/14/30314, FS/13/3/30038 and RG/16/8/32388, and the Cambridge NIHR Biomedical Research Centre.

Author information


  1. Martin R. Bennett and Murray C. H. Clarke are at the Division of Cardiovascular Medicine, University of Cambridge, Box 110 ACCI, Addenbrooke's Hospital, Cambridge, CB2 0QQ, UK.

    • Martin R. Bennett
    •  & Murray C. H. Clarke


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Competing interests

The authors declare no competing financial interests.

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Correspondence to Martin R. Bennett.

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