Fakouri Nima B, Hansen Thomas Lau, Desler Claus, Anugula Sharath, Rasmussen Lene Juel
Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA.
Center for Healthy Aging, Department of Cellular and Molecular Medicine, University of Copenhagen, 2200 Copenhagen, Denmark.
Biology (Basel). 2019 May 11;8(2):35. doi: 10.3390/biology8020035.
In this review we discuss the interaction between metabolic stress, mitochondrial dysfunction, and genomic instability. Unrepaired DNA damage in the nucleus resulting from excess accumulation of DNA damages and stalled replication can initiate cellular signaling responses that negatively affect metabolism and mitochondrial function. On the other hand, mitochondrial pathologies can also lead to stress in the nucleus, and cause sensitivity to DNA-damaging agents. These are examples of how hallmarks of cancer and aging are connected and influenced by each other to protect humans from disease.
在本综述中，我们讨论了代谢应激、线粒体功能障碍和基因组不稳定之间的相互作用。细胞核中由于DNA损伤的过度积累和复制停滞而导致的未修复DNA损伤，可引发对代谢和线粒体功能产生负面影响的细胞信号反应。另一方面，线粒体病变也可导致细胞核应激，并引起对DNA损伤剂的敏感性。这些例子说明了癌症和衰老的特征是如何相互联系和相互影响，以保护人类免受疾病侵害的。
