Mechanism and Regulation of Autophagy and Its Role in Neuronal Diseases

被引：60

作者：

Hu, Zhiping ^{[1
]}

Yang, Binbin ^{[1
]}

Mo, Xiaoye ^{[2
]}

Xiao, Han ^{[1
]}

机构：

[1] Cent S Univ, Xiangya Hosp 2, Dept Neurol, Changsha, Hunan, Peoples R China

[2] Cent S Univ, Xiangya Hosp, Dept Emergency, Changsha, Hunan, Peoples R China

来源：

MOLECULAR NEUROBIOLOGY | 2015年 / 52卷 / 03期

关键词：

Autophagy; Autophagy flux; Neurons; Neurodegenerative diseases; Brain ischemia; Myelin disease; UBIQUITIN-PROTEASOME SYSTEM; AMYOTROPHIC-LATERAL-SCLEROSIS; CHAPERONE-MEDIATED AUTOPHAGY; PROTEIN-KINASE-A; ENDOPLASMIC-RETICULUM; CELL-DEATH; BECLIN; MUTANT HUNTINGTIN; ALPHA-SYNUCLEIN; SPINAL-CORD;

D O I：

10.1007/s12035-014-8921-4

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

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.

引用

页码：1190 / 1209

页数：20

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