Alterungsbedingte Gefäßveränderungen am Beispiel der Arteria carotis

One of the main risk factors for the presence of carotid stenosis and carotid-related stroke is age. The aim of this review article is to present the current state of knowledge on age-related vascular changes using carotid stenosis as an example. Vascular aging (vascular senescence) is a decrease of structural and functional properties of the vessel wall that takes place on different levels. At the multicellular level an increase in vessel volume and diameter as well as intima media thickness occurs with age mainly due to atherosclerotic changes in the vessel wall. At the cellular and extracellular levels there is a decrease in elastin fibers, smooth muscle cells, and total cellularity, an increase in lipid, cholesterol, and calcium phosphate deposition as well as neovascularization. The causes of vascular aging at the molecular level include, in particular oxidative stress, chronic inflammatory response, mitochondrial dysfunction, epigenetic changes, dysregulation of the expression of non-coding RNAs (ncRNAs), and the increase in senescence. Age-related loss of tissue healing and repair capacity make plaques more vulnerable and, in the case of the carotid artery, more susceptible to ischemic stroke. Increasing knowledge of the influence of aging on the epigenetics and ncRNAs in atherosclerotic plaques can in the future more accurately quantify individual patient risk and contribute to the development of targeted therapeutic strategies; however, further studies are needed in this field to understand the full extent of vascular aging and its associated diseases so that these can then be specifically targeted.