[Recent data about the LDL-atherogenesis relationship]

The steps în pathophysiology of ATS make easier the understanding of waves of processes that lead to the disfunction of the endothelial cells, hypertrophy of the arterial wall and în the end to the complication which drawn from this process. Atherogenic process which is characterised by proaterofenethic and atherogenetic mechanism imbalance suppose three phases: early, transition and terminal phase. The initial phase involve the focal influx and LDL-cholesterol accumulation în the arterial intima, the ROS (reactive oxygen species) and azot generation by smooth muscular cells, macrophages and endothelial cells and oxidative modification of LDL. Scientific data revealed that LDL oxidation is mediated by peroxinitrite (ONOO) anion which could act directly over the thiol groups or indirectly through OH and NO radicals from peroxinitrous acid breakdown and who initiate the polyunsaturated fatty acids peroxidation and the oxidation of apolipoprotein B-100. LDL completely oxidated are recognised by scavenger receptors which are not regulated by up and down regulation. The last event of the early atherogenic process is the formation of foam cells from macrophages through LDL modified captation by scavenger receptors.