中国药理学与毒理学杂志Issue(2)：191-201,11.DOI:10.3867/j.issn.1000-3002.2015.02.002
自噬在神经突起变性过程中的作用
Autophagy in neuritic degeneration
摘要
Abstract
Autophagy,an intracellular d egradative pathway,mediates the degradation of long-lived proteins and some cellular organelles and thus plays crucial physiological role in the maintenance of neuronal homeostatsis. The intracellular and extracellular accumulation of protein aggregates is a common pathological alternation in various neurodegenerative disorders. The long and thin axons and dendrites (or collectively “neurites”) are particularly vulnerable to the accumulation of protein aggregates and damaged cellular organelles. Synaptic damage,axonal terminal degeneration,and neuritic atrophy are frequently found in the early stage of neurodegenerative diseases. Therefore, efficient clearance of protein aggregates and damaged cellular organelles by autophagic pathway may suppress neuritic degeneration. However, it is also demonstrated that insufficient autophagy or excessive autophagic activation contributes to neuritic injury. Here,the recent advances in the study of neuritic autophagy have been reviewed. We firstly introduce the biogenesis and transport of autophagosomes in neurites. Secondly,the regulatory role of autophagy in neuritic growth and damage is reviewed. Finally,the association between autophagy and neurodegenerative diseases is discussed.关键词
自噬/神经变性疾病/轴突/树突Key words
autophagy/neurodegenerative disease/axon/dendrite分类
医药卫生引用本文复制引用
杨怡,王姗姗,魏尔清,张丽慧..自噬在神经突起变性过程中的作用[J].中国药理学与毒理学杂志,2015,(2):191-201,11.基金项目
国家自然科学基金（81401043）；国家自然科学基金（81273491）；浙江省自然科学基金（LQ13H310004）；浙江省自然科学基金（LY12H31010）；浙江省医药卫生一般研究计划（2013KYA147）；杭州市重点实验室项目（20090233T12）；杭州师范大学科研启动经费项目（2012QDL048）@@@@The project supported by National Natural Science Foundation of China （81401043）；National Natural Science Foundation of China （81273491）； Zhejiang Provincial Natural Science Foundation of China （LQ13H310004）；Zhejiang Provincial Natural Science Foundation of China （LY12H31010）；Health Bureau of Zhejiang Province （2013KYA147）；the Key Laboratory of Hangzhou City Project （20090233T12）；and Science Foundation of Hangzhou Normal University （）
