Genetic Mutations and Mitochondrial Toxins Shed New Light on the Pathogenesis of Parkinson's Disease

Figure 1

Schematic representation of PINK1-parkin-mediated mitophagy. In damaged mitochondria, PINK1 and parkin regulate mitochondrial elimination by inducing mitophagy. Under steady state, PINK1 is cleaved and degraded rapidly in the mitochondria. This process may be inhibited by the mitochondrial depolarization, resulting in PINK1 accumulation in the mitochondria. This accumulation is a crucial signal for parkin recruitment to the mitochondria. Parkin is presumed to ubiquitinate substrate (X), resulting in the induction of mitophagy.