Mitophagy: the latest problem for Parkinson's disease

被引:114
|
作者
Vives-Bauza, Cristofol [1 ]
Przedborski, Serge [1 ,2 ,3 ]
机构
[1] Columbia Univ, Dept Neurol, New York, NY 10027 USA
[2] Columbia Univ, Dept Pathol & Cell Biol, New York, NY USA
[3] Columbia Univ, Ctr Motor Neuron Biol & Dis, New York, NY USA
关键词
CHAPERONE-MEDIATED AUTOPHAGY; ALPHA-SYNUCLEIN; CELL-DEATH; MITOCHONDRIAL AUTOPHAGY; RECESSIVE PARKINSONISM; SELECTIVE AUTOPHAGY; PINK1; MUTATIONS; PROTEIN; DEGRADATION;
D O I
10.1016/j.molmed.2010.11.002
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Parkinson's disease (PD) is a common neurodegenerative disorder of unknown cause. Some familial forms of PD are provoked by mutations in the genes encoding for the PTEN (phosphatase and tensin homolog)-induced putative kinase-1 (PINK1) and Parkin. Mounting evidence indicates that PINK1 and Parkin might function in concert to modulate mitochondrial degradation, termed mitophagy. However, the molecular mechanisms by which PINK1/Parkin affect mitophagy are just beginning to be elucidated. Herein, we review the main advances in our understanding of the PINK1/Parkin pathway. Because of the phenotypic similarities among the different forms of PD, a better understanding of PINK1/Parkin biology might have far-reaching pathogenic and therapeutic implications for both the inherited and the sporadic forms of PD.
引用
收藏
页码:158 / 165
页数:8
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