• Open Access

Is cellular senescence an example of antagonistic pleiotropy?

Authors

  • Stefano Giaimo,

    1. IFOM Foundation – The FIRC Institute of Molecular Oncology Foundation via Adamello 16, 20139 Milan, Italy
    2. SEMM – European School of Molecular Medicine via Adamello 16, 20139 Milan, Italy
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  • Fabrizio d’Adda di Fagagna

    1. IFOM Foundation – The FIRC Institute of Molecular Oncology Foundation via Adamello 16, 20139 Milan, Italy
    2. Istituto di Genetica Molecolare-Consiglio Nazionale delle Ricerche, Via Abbiategrasso 207, 27100 Pavia, Italy
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Fabrizio d’Adda di Fagagna, IFOM Foundation – The FIRC Institute of Molecular Oncology Foundation, via Adamello 16, 20139 Milan, Italy. Tel. +39 02 574303 227; fax +39 02 574303 231; e-mail: fabrizio.dadda@ifom-ieo-campus.it

Summary

It is generally accepted that the permanent arrest of cell division known as cellular senescence contributes to aging by an antagonistic pleiotropy mechanism: cellular senescence would act beneficially early in life by suppressing cancer, but detrimentally later on by causing frailty and, paradoxically, cancer. In this review, we show that there is room to rethink this common view. We propose a critical appraisal of the arguments commonly brought in support of it, and we qualitatively analyse published results that are of relevance to understand whether or not cellular senescence-associated genes really act in an antagonistic-pleiotropic manner in humans.

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