Research Paper Volume 8, Issue 10 pp 2355—2369

Figure 8. Schematic diagram summarizing the control of mitochondrial functions by caveolin-1 through the regulation of AFG3L2. Under resting conditions (-ROS), both wild type and caveolin-1 null cells possess functional respiratory chain complexes and generate energy mostly through oxidative phosphorylation. Upon oxidative stress, the caveolin-1-dependent localization of AFG3L2 to mitochondria in wild type cells prevents ROS-mediated mitochondrial damage by providing mitochondrial protein quality control. As a consequence, functional respiratory chain complexes are maintained. After oxidative stress but in the absence of caveolin-1, AFG3L2 fails to localize to mitochondria and the AFG3L2-mediated protective mechanism is lost, leading to the degradation of respiratory chain proteins. Under these conditions, oxidative phosphorylation is impaired and caveolin-1 null cells rely on enhanced glycolysis for their bioenergetic requirements.