Mitochondrial quality control and Parkinson's disease: a pathway unfolds.
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.
Cell Death Regulation Laboratory, MRC Toxicology Unit, Hodgkin Building, Lancaster Road, Leicester, LE1 9HN, UK.
Inês Pimenta
IP
de Castro
L Miguel
LM
Martins
Samantha Hui Yong
SH
Loh
D000818:Animals; D004195:Disease Models, Animal; D006801:Humans; D008928:Mitochondria / Q000378:metabolism* / Q000473:pathology*; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D010300:Parkinson Disease / Q000201:enzymology / Q000235:genetics / Q000378:metabolism* / Q000473:pathology*; D011494:Protein Kinases / Q000378:metabolism; D000099202:PTEN-Induced Putative Kinase
D011494:Protein Kinases; D000099202:PTEN-Induced Putative Kinase