Yu Emma P K, Bennett Martin R
Division of Cardiovascular Medicine, University of Cambridge, Box 110, Addenbrooke's Centre for Clinical Investigation, Addenbrooke's Hospital, Cambridge CB2 2QQ, United Kingdom.
Division of Cardiovascular Medicine, University of Cambridge, Box 110, Addenbrooke's Centre for Clinical Investigation, Addenbrooke's Hospital, Cambridge CB2 2QQ, United Kingdom.
Free Radic Biol Med. 2016 Nov;100:223-230. doi: 10.1016/j.freeradbiomed.2016.06.011. Epub 2016 Jun 16.
Mitochondria are the cellular powerhouses, fuelling metabolic processes through their generation of ATP. However we now recognise that these organelles also have pivotal roles in producing reactive oxygen species (ROS) and in regulating cell death, inflammation and metabolism. Mitochondrial dysfunction therefore leads to oxidative stress, cell death, metabolic dysfunction and inflammation, which can all promote atherosclerosis. Recent evidence indicates that mitochondrial DNA (mtDNA) damage is present and promotes atherosclerosis through mitochondrial dysfunction. We will review the mechanisms that link mtDNA damage with atherosclerotic disease, and identify mitochondrial processes that may have therapeutic benefit.
线粒体是细胞的动力源，通过产生三磷酸腺苷（ATP）为代谢过程提供能量。然而，我们现在认识到这些细胞器在产生活性氧（ROS）以及调节细胞死亡、炎症和代谢方面也起着关键作用。因此，线粒体功能障碍会导致氧化应激、细胞死亡、代谢功能障碍和炎症，所有这些都可能促进动脉粥样硬化。最近的证据表明，线粒体DNA（mtDNA）损伤存在，并通过线粒体功能障碍促进动脉粥样硬化。我们将综述将mtDNA损伤与动脉粥样硬化疾病联系起来的机制，并确定可能具有治疗益处的线粒体过程。
