Graduate Center for Toxicology, 454 HSRB, University of Kentucky, Lexington, KY 40536, USA.
Curr Pharm Biotechnol. 2013;14(3):261-73. doi: 10.2174/1389201011314030003.
Accumulated evidence suggests that p53 plays an important role in the regulation of metabolism and intracellular redox homeostasis through transcription-dependent and -independent mechanisms. Mitochondria, the power plant of cells, provide cells with ATP for their functions by regulating energy metabolism. In addition, as the byproducts of metabolism, reactive oxygen species (ROS) generated in the mitochondria can serve as signaling molecules to regulate p53 function. The regulation of p53 by mitochondria, especially redox-mediated regulation, may be involved in controlling the cellular switch between survival and death. The interplay between p53 and manganese superoxide dismutase (MnSOD), an important mitochondrial antioxidant enzyme, is an example of how nuclear and mitochondrial p53 coordinate their response to different levels of stress and contribute to the fate of cells.
积累的证据表明,p53 通过转录依赖和非依赖机制在代谢和细胞内氧化还原稳态的调节中发挥重要作用。线粒体是细胞的“发电站”,通过调节能量代谢为细胞的功能提供 ATP。此外,作为代谢的副产物,在线粒体中产生的活性氧(ROS)可以作为信号分子来调节 p53 的功能。线粒体对 p53 的调节,特别是氧化还原介导的调节,可能参与控制细胞在存活和死亡之间的转换。p53 与锰超氧化物歧化酶(MnSOD)之间的相互作用,MnSOD 是一种重要的线粒体抗氧化酶,就是核和线粒体 p53 如何协调对不同水平的应激的反应,并有助于细胞命运的一个例子。