[Glucose, glycotoxins, and protein glycation products: the role in pathogensis]

Arteriosclerosis and atheromatosis are etiologically and pathogenetically different non-physiological processes in atherosclerosis localized in the proximal segments of the arterial bed and elastic-type arteries; both affect the structure and function of the arterial wall. They cause an inflammatory reaction with subsequent compaction (sclerosing) of the walls of large and mid-size arteries, the loss of their elasticity due to structural changes in the loose connective tissue of intima-media, impaired elasticity and enhanced rigidity of the wall, inflammation, fibrosis, and increased pulse wave conduction velocity. Arteriosclerosis is initiated by long-term hyperglycemia, chemical collagen and elastin glycation by glucose and its metabolites (glycotoxins glyoxal and methylglyoxal) forming cross-links between collagen and elastin fibers. In contrast, atheromatosis as the main manifestation of atherosclerosis affects elastic-type arteries via accumulation of intimal lipids (cholesterol-esterified essential unsaturated and polyenic fatty acids, plaque formation at the sites of macrophage deposition in intima, necrotic and calcinotic foci. Atheromatosis does not affect collageous and elastic structures in the arterial wall. Arteriosclerosis and atheromatosis are two independent pathological processes in the walls of elastic-type arteries. Arteriosclerosis results from glycation of collagen and elastin chains in muscular-type arterioles, postarterioles, endothelium, and pericytes of exchangeable capillaries. Microangiopathy initiates only glycation and glycotoxin action because muscular-type arterioles have no intima, an interstitial tissue for the collection and utilization of biological "rubbish" from blood and intravascular pool of intercellular medium.