Mitochondrial Quality Control and Parkinson's Disease: A Pathway Unfolds

被引：53

作者：

de Castro, Ines Pimenta ^{[1
,2
,3
]}

Martins, L. Miguel ^{[1
]}

Loh, Samantha Hui Yong ^{[1
]}

机构：

[1] MRC, Toxicol Unit, Cell Death Regulat Lab, Leicester LE1 9HN, Leics, England

[2] Univ Porto, IPATIMUP, P-4100 Oporto, Portugal

[3] Univ Porto, Fac Pharm, P-4100 Oporto, Portugal

来源：

MOLECULAR NEUROBIOLOGY | 2011年 / 43卷 / 02期

基金：

英国医学研究理事会;

关键词：

Mitochondria; PINK1; HtrA2; Parkin; Parkinson's disease; Unfolded proteins; SERINE-PROTEASE HTRA2/OMI; CELL-DEATH; STRESS; PINK1; MUTATIONS; AUTOPHAGY; NEURODEGENERATION; DROSOPHILA-PINK1; DYSFUNCTION; SURVIVAL;

D O I：

10.1007/s12035-010-8150-4

中图分类号：

Q189 [神经科学];

学科分类号：

071006 [神经生物学];

摘要：

Recent findings from genetic studies suggest that defective mitochondrial quality control may play an important role in the development of Parkinson's disease (PD). Such defects may result in the impairment of neuronal mitochondria, which leads to both synaptic dysfunction and cell death and results in neurodegeneration. Here, we review state-of-the-art knowledge of how pathways affecting mitochondrial quality control might contribute to PD, with a particular emphasis on the molecular mechanisms employed by PTEN-induced putative kinase 1 (PINK1), HtrA2 and Parkin to regulate mitochondrial quality control.

引用

页码：80 / 86

页数：7

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