Figure 1.

A theoretical graphic representation and overview of PINK1, Parkin, and related molecules in regulatory pathway for mitophagy. Under the healthy and steady state of cells, PINK1 is degraded within the surface of the mitochondria. This may be subdued by mitochondrial damage due to oxidative stress, resulting in PINK1 and Parkin accumulation in the outer membrane of mitochondria. PINK1 could phosphorylate ubiquitin to activate Parkin ubiquitin ligase activity. In addition, the Parkin is also assumed to be phosphorylated and ubiquitinated, resulting in the induction of mitophagy. Note that some critical pathways have been omitted for clarity. OMM, outer mitochondrial membrane; IMM, inner mitochondrial membrane; MARK2, microtubule affinity regulating kinase 2; MFN1, mitofusin 1; MFN2, mitofusin 2; NDP52, nuclear dot protein 52; PARL, presenilin-associated rhomboid-like; OPTN, optineurin; PINK1, PTEN-induced kinase 1; VDAC1, voltage-dependent anion channel 1; Ub, ubiquitin.