Figure 1. Compensation of mtQC impairments. Loss of mitochondrial superoxide dismutase PaSOD3 leads to unspecific damage of all kinds of molecules (red stars) by ROS. This damage, as long as it is not excessive, does not significantly effect ATP generation. Within certain limits, the accumulation of damage can be compensated by induction of mitophagy and mitochondrial biogenesis, leading to a remodeling and/or substitution of damaged mitochondria and a wild-type-like lifespan. In contrast, ablation of the mitochondrial PaCLPXP leads to impaired mitochondrial respiration complexes and other enzymes of the energy metabolism (light grey). This impairment can be compensated by a response leading to the induction of alternative oxidase (AOX) and by upregulation of general autophagy and results in the conservation of a wild-type-like ATP content.