PINK1 deficiency enhances autophagy and mitophagy induction

Rubén Gómez-Sánchez, Sokhna M S Yakhine-Diop, José M Bravo-San Pedro, Elisa Pizarro-Estrella, Mario Rodríguez-Arribas, Vicente Climent, Francisco E Martin-Cano, María E González-Soltero, Anurag Tandon, José M Fuentes*, Rosa A González-Polo

*Corresponding author voor dit werk

    OnderzoeksoutputAcademicpeer review

    19 Citaten (Scopus)


    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.

    Originele taal-2English
    Aantal pagina's10
    TijdschriftMolecular & Cellular Oncology
    Nummer van het tijdschrift2
    StatusPublished - 2016


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