Journal
MOLECULAR & CELLULAR ONCOLOGY
Volume 3, Issue 2, Pages -Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/23723556.2015.1046579
Keywords
autophagy; cancer; mitochondria; mitophagy; Parkinson's disease; PINK1
Categories
Funding
- Instituto de Salud Carlos III [PI11/00040, PI12/02280, PI14/00170, CB06/05/0041]
- European Union FEDER funds
- Gobierno de Extremadura [GR10054]
- Universidad de Extremadura, Spain
- CIBERNED, Instituto de Salud Carlos III, Spain
- FPU predoctoral fellowship (Ministerio de Educacion, Cultura y Deporte, Spain)
- RETICEF [RD12-0043-0016]
- Parkinson Society of Canada
- Canadian Institutes of Health Research
- Gobierno de Extremadura, Spain
- [BFU2011-24365]
- [GR 10009 JEX]
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Parkinson's disease (PD) is a neurodegenerative disorder with poorly understood etiology. Increasing evidence suggests that age-dependent compromise of the maintenance of mitochondrial function is a key risk factor. Several proteins encoded by PD-related genes are associated with mitochondria including PTEN-induced putative kinase 1 (PINK1), which was first identified as a gene that is upregulated by PTEN. Loss-of-function PINK1 mutations induce mitochondrial dysfunction and, ultimately, neuronal cell death. To mitigate the negative effects of altered cellular functions cells possess a degradation mechanism called autophagy for recycling damaged components; selective elimination of dysfunctional mitochondria by autophagy is termed mitophagy. Our study indicates that autophagy and mitophagy are upregulated in PINK1-deficient cells, and is the first report to demonstrate efficient fluxes by one-step analysis. We propose that autophagy is induced to maintain cellular homeostasis under conditions of non-regulated mitochondrial quality control.
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