Kim Dah Ihm, Lee Ki Hoon, Oh Ji Young, Kim Jun Sung, Han Ho Jae
Department of Veterinary Physiology, College of Veterinary Medicine, Research Institute for Veterinary Science, Seoul National University, Seoul, 08826, South Korea.
Department of Agricultural Biotechnology, Animal Biotechnology Major, and Research Institute of Agriculture and Life Science, Seoul National University, Seoul, 08826, South Korea.
Cell Mol Neurobiol. 2017 Aug;37(6):955-968. doi: 10.1007/s10571-016-0434-4. Epub 2016 Oct 20.
Mitochondria as dynamic organelles undergo morphological changes through the processes of fission and fusion which are major factors regulating their functions. A disruption in the balance of mitochondrial dynamics induces functional disorders in mitochondria such as failed energy production and the generation of reactive oxygen species, which are closely related to pathophysiological changes associated with Alzheimer's disease (AD). Recent studies have demonstrated a relationship between abnormalities in mitochondrial dynamics and impaired mitochondrial function, clarifying the effects of morphofunctional aberrations which promote neuronal cell death in AD. Several possible signaling pathways have been suggested for a better understanding of the mechanism behind the key molecules regulating mitochondrial morphologies. However, the exact machinery involved in mitochondrial dynamics still has yet to be elucidated. This paper reviews the current knowledge on signaling mechanisms involved in mitochondrial dynamics and the significance of mitochondrial dynamics in controlling associated functions in neurodegenerative diseases, particularly in AD.
线粒体作为动态细胞器,通过裂变和融合过程发生形态变化,而这两个过程是调节其功能的主要因素。线粒体动力学平衡的破坏会诱导线粒体功能紊乱,如能量产生失败和活性氧的生成,这些都与阿尔茨海默病(AD)相关的病理生理变化密切相关。最近的研究表明线粒体动力学异常与线粒体功能受损之间存在关联,阐明了形态功能异常促进AD中神经元细胞死亡的作用。为了更好地理解调节线粒体形态的关键分子背后的机制,已经提出了几种可能的信号通路。然而,参与线粒体动力学的确切机制仍有待阐明。本文综述了目前关于线粒体动力学相关信号机制的知识,以及线粒体动力学在控制神经退行性疾病,特别是AD相关功能中的意义。