Altered mitochondrial energy metabolism may play a role in vascular aging.

Epidemiological studies demonstrated that even in the absence of other risk factors (e.g., diabetes, hypertension, hypercholesterolemia), vascular aging significantly increases cardiovascular morbidity. Previous studies revealed that vascular aging is characterized by an age-dependent decline in endothelial function due to a decreased bioavailability of NO and increased production of reactive oxygen species. Yet, the mechanisms underlying the process of vascular aging are still poorly understood. Many authors consider that aging is a mitochondrial disease. Indeed, there is evidence that aging is associated with an increase in mtDNA damage and a decline in expression/activity of mitochondrial enzymes in various organs. On the basis of recent observations we predict that similar changes in mitochondrial gene expression profile are present in the aged cardiovascular system as well. It is significant, that components of the electron transport chain (including cytochrome c oxidase) seem to be similarly down-regulated with age in many species. Because pharmacological inhibition of mitochondrial energy metabolism significantly impairs endothelium-dependent vascular relaxation and may increase the production of reactive oxygen species, we propose that alterations of mitochondrial energetic phenotype may contribute to endothelial dysfunction in aging.