Mitophagy: the latest problem for Parkinson's disease

• Published in: Trends in molecular medicine 2011-03, Vol.17 (3), p.158-165
• Main Authors: Vives-Bauza, Cristofol, Przedborski, Serge
• Format: Article
• Language: English
• Subjects: Animals; Autophagy; Humans; Mitochondria - enzymology; Mitochondria - genetics; Mitochondria - metabolism; Parkinson Disease - enzymology; Parkinson Disease - genetics; Parkinson Disease - physiopathology; Pathology; Protein Kinases - genetics; Protein Kinases - metabolism; Ubiquitin-Protein Ligases - genetics; Ubiquitin-Protein Ligases - metabolism
• ISSN: 1471-4914; 1471-499X
• DOI: 10.1016/j.molmed.2010.11.002

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.