Clinical Relevance of Advanced Glycation Endproducts for Vascular Surgery

Extracellular advanced glycation endproducts (AGEs) may bind several proteins, including lipids and collagen. The crosslinking of collagen increases vascular stiffness and alters the extracellular matrix. The binding of AGEs to RAGE on e.g. endothelial cells induces a signaling cascade with nuclear factor kappa beta (NF-kB) as key signaling factor. NF-kB increases the transcription of different proteins, including endothelin-1, ICAM (intercellular adhesion molecule), VCAM (vascular cell adhesion molecule), TNF-alpha (tumour necrosis factor) and interleukines (IL). This cascade aggravates vascular inflammation and the production of ROS (reactive oxygen species). Furthermore, AGE–RAGE interaction induces endothelial dysfunction by its effect on endothelial nitric oxide (NO) synthase (eNOS). AGEs activate monocytes, causing increased expression of CD36 receptors leading to increased AGE-lipid (e.g. AGE-LDL) uptake and foam cell formation.

(A) The Autofluorescence Reader illuminates a skin surface with an excitation light source between 300–420nm. Only light from the skin is measured with a spectrometer. (B) Various fluorescence spectrum results from different subjects: healthy subject (black line), diabetic patient without cardiovascular complications (blue line), diabetic patient with peripheral artery occlusive disease (green line), hemodialysis patient with recent myocardial infarction (red line). I=intensity (a.u.).