[Reactivity of the arterial wall to atherogenic stimuli]

Our understanding of the biological mechanism implicated in spontaneous or accelerated atherogenesis is steadily increasing. The vascular response to atherogenic stimuli implies activation of endothelial cells making possible the adhesion and then the migration of circulating mononuclear cells. When these cells are present in the intima they participate in the production of a number of factors liable to activate the migration and proliferation of the underlying smooth muscle cells (cytokines, growth factors, physiologically active lipids). The rupture of parietal homeostasis is discussed with reference to some experimental models in terms of intimal cellular recruitment and formation of foam cells which are the cardinal points of the initial pathogenic process.