IFOM Foundation -- The FIRC Institute of Molecular Oncology Foundation via Adamello 16, 20139 Milan, Italy.
Aging Cell. 2012 Jun;11(3):378-83. doi: 10.1111/j.1474-9726.2012.00807.x. Epub 2012 Mar 15.
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.
普遍认为，细胞分裂的永久停滞，即细胞衰老，通过拮抗多效性机制导致衰老：细胞衰老在生命早期通过抑制癌症发挥有益作用，但后来会导致脆弱，并矛盾地导致癌症。在这篇综述中，我们表明有重新思考这一普遍观点的空间。我们对支持这一观点的常见论点进行了批判性评估，并对相关的已发表结果进行了定性分析，以了解细胞衰老相关基因是否真的在人类中以拮抗多效性方式发挥作用。
