Oxidative stress in endothelial cells and in diabetes type 2

Reactive oxygen species (ROS) are important signaling molecules in human cells. At physiological concentrations, they can for instance protect against apoptosis and act as secondary messengers in many different signaling pathways. Disturbance of redox homeostasis, i.e., the physiological balance between ROS generation and degradation, leads to not only increased ROS levels, so-called oxidative stress, but also results in damage to macromolecules and promotes the development of diseases and accelerates the aging process. The organism has various enzyme systems at hand to eliminate excess ROS. Their inactivation or degradation under conditions of oxidative stress is tightly linked to endothelial dysfunction due to endothelial cell apoptosis, a loss of telomerase activity, and telomere shortening. Restricted endothelial function causes cardiovascular diseases and diabetes type 2.