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Updated: Jun 6, 2026

The Use of Primary Human Fibroblasts for Monitoring Mitochondrial Phenotypes in the Field of Parkinson's Disease
Published on: October 3, 2012
Mitochondrial quality control and Parkinson's disease: a pathway unfolds
Inês Pimenta de Castro1, L Miguel Martins, Samantha Hui Yong Loh
1Cell Death Regulation Laboratory, MRC Toxicology Unit, Hodgkin Building, Lancaster Road, Leicester, LE1 9HN, UK.
None:
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.
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