Selvaraji Sharmelee, Poh Luting, Natarajan Venkateswaran, Mallilankaraman Karthik, Arumugam Thiruma V
Department of Physiology, Yong Loo Lin School Medicine, National University of Singapore, Singapore.
NUS Graduate School for Integrative Sciences and Engineering, National University of Singapore, Singapore.
Cond Med. 2019 Feb;2(1):30-39.
Mitochondrial dysfunction is regarded as one of the major causes of neuronal injury in age-associated neurodegenerative diseases and stroke. Mitochondrial dysfunction leads to increased reactive oxygen species production, causing mitochondrial DNA mutations, which then results in pathological conditions. Negative conditioning of mitochondrial dysfunction via pharmacological inhibition, phytochemicals, and dietary restriction serve as an avenue for therapeutic intervention to improve mitochondrial quality and function. Here, we focus primarily on mitochondrial biology, evidence for mitochondrial dysfunction in neurodegenerative conditions such as dementia and stroke, and the possibility of using negative conditioning to restore or preserve mitochondrial function in these diseases.
线粒体功能障碍被认为是与年龄相关的神经退行性疾病和中风中神经元损伤的主要原因之一。线粒体功能障碍导致活性氧生成增加，引发线粒体DNA突变，进而导致病理状况。通过药物抑制、植物化学物质和饮食限制对线粒体功能障碍进行负调控，为改善线粒体质量和功能的治疗干预提供了一条途径。在这里，我们主要关注线粒体生物学、痴呆和中风等神经退行性疾病中线粒体功能障碍的证据，以及在这些疾病中利用负调控恢复或维持线粒体功能的可能性。
