ABSTRACT
Recent data suggest that defective, unneeded, and senescing mitochondria generate toxic by-products, especially reactive oxygen species (ROS), threatening themselves, neighboring mitochondria, and the host cell. Toxic mitochondria arise continuously with aging and are eliminated by the process of mitophagy. Mitochondria marked for degradation are fenced off by encirclement with a membranous structure that fuses with a lysozome where digestion proceeds. A detailed description of the biochemistry of mitophagy is beyond the scope of this book. Our interest focuses on the physiological benets of mitophagy, especially in degrading toxic mitochondria and preventing oxidative and energy stress. Obviously, mitophagy rids the cell of severely oxidatively damaged membranes, in essence eliminating a major source of ROS.
