Corneal scattering and biomechanical behavior in eyes with Fuchs' endothelial dystrophy

aerobic respiration generates reactive oxygen species (ROS) as a byproduct. ROS are needed for regulating signal transduction in cells, and they promote also the production of pro-inflammatory cytokines. In normal conditions, cells have various antioxidants keeping the ROS levels in balance. In aged cells, antioxidative systems deteriorate and ROS production accelerates, which together result in excessive ROS levels. This oxidative stress has been associated with numerous inflammatory diseases. Aged mitochondria are efficient in producing ROS, and those organelles should be removed by autophagy. However, aging impairs autophagy, which further enables the excessive ROS production by damaged mitochondria. This creates a vicious circle where impaired autophagy, dysfunctional mitochondria, are inflammation are central players regulating each other.