Mitochondrial dysfunction and cell senescence: deciphering a complex relationship
Mitochondrial dysfunction and cell senescence: deciphering a complex relationship
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DOI：
10.1002/1873-3468.13498
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发表时间：
2019-07-01
期刊：
影响因子：
3.5
通讯作者：
Passos, Joao F.
中科院分区：
文献类型：
--
作者：
Chapman, James;Fielder, Edward;Passos, Joao F.
细胞衰老和线粒体功能障碍都被定义为衰老过程的典型特征。在这里，我们将回顾两者之间错综复杂的关系。在老龄化的背景下，现在人们普遍认为，细胞衰老是衰老和一些与年龄有关的疾病发生的关键驱动因素。越来越多的证据表明线粒体是衰老表型，特别是促炎性衰老相关分泌表型(SASP)的关键调节因子之一。这篇综述着重于体内平衡机制的贡献，以及活性氧和线粒体代谢物在衰老过程中的作用。此外，我们还讨论了可能影响SASP的新出现的途径和线粒体介导的机制，并随后探索了如何利用这些途径来开辟新的治疗途径。
Cellular senescence and mitochondrial dysfunction have both been defined as classical hallmarks of the ageing process. Here, we review the intricate relationship between the two. In the context of ageing, it is now well regarded that cellular senescence is a key driver in both ageing and the onset of a number of age-related pathologies. Emerging evidence has pinpointed mitochondria as one of the key modulators in the development of the senescence phenotype, particularly the pro-inflammatory senescence associated secretory phenotype (SASP). This review focuses on the contribution of homeostatic mechanisms, as well as of reactive oxygen species and mitochondrial metabolites in the senescence programme. Furthermore, we discuss emerging pathways and mitochondrial-mediated mechanisms that may be influencing the SASP and, subsequently, explore how these may be exploited to open up new therapeutic avenues.