Ubiquitin and Receptor-Dependent Mitophagy Pathways and Their Implication in Neurodegeneration

Abstract

Selective autophagy of mitochondria, or mitophagy, refers to the specific removal and degradation of damaged or surplus mitochondria via targeting to the lysosome for destruction. Disruptions in this homeostatic process may contribute to disease. The identification of diverse mitophagic pathways and how selectivity for each of these pathways is conferred is just beginning to be understood. The removal of both damaged and healthy mitochondria under disease and physiological conditions is controlled by either ubiquitin-dependent or receptor-dependent mechanisms. In this review, we will discuss the known types of mitophagy observed in mammals, recent findings related to PINK1/Parkin-mediated mitophagy (which is the most well-studied form of mitophagy), the implications of defective mitophagy to neurodegenerative processes, and unanswered questions inspiring future research that would enhance our understanding of mitochondrial quality control.

Keywords: Autophagosome; BNIP3L/Nix; Mitochondria; PINK1/Parkin; Ubiquitin.