Hu Zhiping, Yang Binbin, Mo Xiaoye, Xiao Han
Departement of Neurology, 2nd Xiangya Hospital, Central South University, Changsha, China.
Departement of Emergency, Xiangya Hospital, Central South University, Changsha, China.
Mol Neurobiol. 2015 Dec;52(3):1190-1209. doi: 10.1007/s12035-014-8921-4. Epub 2014 Oct 15.
Autophagy is a constitutive lysosomal catabolic pathway that degrades damaged organelles and protein aggregates. Neuronal survival is highly dependent on autophagy due to its post-mitotic nature, polarized morphology, and active protein trafficking. Autophagic dysfunction has been linked to several neuronal diseases. Our understanding is still incomplete but may highlight up-to-date findings on how autophagy is executed and regulated at the molecular level and its role in neurodegenerative diseases (including Alzheimer's disease (AD), Huntington's disease (HD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS)), brain ischemia, and myelin diseases, hence providing attractive new avenues for the development of treatment strategies to combat neuronal diseases.
自噬是一种组成性的溶酶体分解代谢途径,可降解受损的细胞器和蛋白质聚集体。由于神经元具有有丝分裂后特性、极化形态和活跃的蛋白质运输,其存活高度依赖于自噬。自噬功能障碍与多种神经疾病有关。我们的理解仍不完整,但可能会突出关于自噬在分子水平上如何执行和调控及其在神经退行性疾病(包括阿尔茨海默病(AD)、亨廷顿病(HD)、帕金森病(PD)、肌萎缩侧索硬化症(ALS))、脑缺血和髓鞘疾病中的作用的最新发现,从而为开发对抗神经疾病的治疗策略提供有吸引力的新途径。