摘要
线粒体功能障碍在肌萎缩侧索硬化(ALS)的发病中有着重要作用。线粒体功能障碍导致严重的氧化应激损伤和细胞钙稳态失衡,以及被异常释放的线粒体DNA激活炎性反应,这些可能是造成ALS患者运动神经元死亡的重要原因。线粒体自噬作为线粒体质量控制的最后环节,其功能的减弱或过度增强都会促进ALS的发展。
Mitochondrial dysfunction plays an important role in the pathogenesis of amyotrophic lateral sclerosis(ALS).The mitochondrial dysfunction will cause severe oxidative stress and disruption in calcium homeostasis.The abnormally released mitochondrial DNA will induce cellular inflammation.These phenomena may explain the loss of motor neurons in ALS patients.As a quality control process,either abnormal increased or decreased mitophagy flux will speed up the pathogenic development of ALS.
作者
刘立洋
柳青
刘雅萍
张学
LIU Liyang;LIU Qing;LIU Yaping;ZHANG Xue(Department of Medical Genetics,Institute of Basic Medical Sciences CAMS,School of Basic Medicine PUMC,Beijing 100005;Department of Neurology,Peking Union Medical College Hospital,Chinese Academy of Medical Sciences&Peking Union Medical College,Beijing 100730;4+4 Medical Doctor Program,Chinese Academy of Medical Sciences&Peking Union Medical College,Beijing 100730,China)
出处
《基础医学与临床》
2023年第2期332-335,共4页
Basic and Clinical Medicine
基金
中国医学科学院医学与健康科技创新工程(2021-I2M-1-018)。
关键词
肌萎缩侧索硬化
线粒体功能障碍
amyotrophic lateral sclerosis
mitochondrial dysfunction
