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Review
. 2013 Sep 15;126(Pt 18):4061-7.
doi: 10.1242/jcs.109728. Epub 2013 Aug 22.

Senescence at a glance

Affiliations
Review

Senescence at a glance

Jeff S Pawlikowski et al. J Cell Sci. .

Abstract

Cellular senescence is a stable proliferation arrest that is associated with extensive cellular remodelling and an altered secretory pathway. Through its numerous inducers that lead to altered gene expression, senescence is able to influence many contrasting functions and pathologies, namely tumour suppression, tumour promotion, wound healing and ageing. As senescence is able to control such important tissue functions, it is now being pinpointed as a possible route for novel therapies. This article and accompanying poster aim to provide a summary of the initiators, pathways and roles of senescence, as well as present examples of senescence and a possible use for senescence in therapy.

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References

    1. Acosta J. C., O'Loghlen A., Banito A., Guijarro M. V., Augert A., Raguz S., Fumagalli M., Da Costa M., Brown C., Popov N. et al.(2008). Chemokine signaling via the CXCR2 receptor reinforces senescence. Cell 133, 1006–1018 10.1016/j.cell.2008.03.038 - DOI - PubMed
    1. 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). A complex secretory program orchestrated by the inflammasome controls paracrine senescence. Nat. Cell Biol doi: 10.1038/ncb2784 - PMC - PubMed
    1. Adams P. D. (2009). Healing and hurting: molecular mechanisms, functions, and pathologies of cellular senescence. Mol. Cell 36, 2–14 10.1016/j.molcel.2009.09.021 - DOI - PubMed
    1. Baker D. J., Perez-Terzic C., Jin F., Pitel K. S., Niederländer N. J., Jeganathan K., Yamada S., Reyes S., Rowe L., Hiddinga H. J. et al.(2008). Opposing roles for p16Ink4a and p19Arf in senescence and ageing caused by BubR1 insufficiency. Nat. Cell Biol. 10, 825–836 10.1038/ncb1744 - DOI - PMC - PubMed
    1. Baker D. J., Wijshake T., Tchkonia T., LeBrasseur N. K., Childs B. G., van de Sluis B., Kirkland J. L., van Deursen J. M. (2011). Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders. Nature 479, 232–236 10.1038/nature10600 - DOI - PMC - PubMed

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