Department of Biochemistry and Molecular Medicine, Université de Montréal, C.P. 6128, Succ. Centre-Ville, Montréal, Québec H3C 3J7, Canada.
Exp Gerontol. 2018 Jul 1;107:50-54. doi: 10.1016/j.exger.2017.06.016. Epub 2017 Jun 27.
Senescent cells accumulate with age and contribute to pathologies associated to old age. The senescent program can be induced by pro-cancer stimuli or is developmentally controlled. In cells forced to senesce by expression of oncogenes or short telomeres, aberrant activation of the ERK/MAP kinase signaling pathway leads to selective protein degradation by the ubiquitin proteasome system. The proteins affected by this process control key cellular processes known to be defective in senescent cells. We discuss the evidence supporting a general role for aberrant signaling and senescence associated protein degradation for organismal aging.
衰老细胞随着年龄的增长而积累，并导致与老年相关的病理。衰老程序可以被致癌刺激物诱导，也可以被发育控制。在通过表达致癌基因或短端粒而被迫衰老的细胞中，ERK/MAP 激酶信号通路的异常激活导致泛素蛋白酶体系统对选择性蛋白质的降解。受这一过程影响的蛋白质控制着已知在衰老细胞中存在缺陷的关键细胞过程。我们讨论了支持异常信号和与衰老相关的蛋白质降解在机体衰老中普遍作用的证据。
