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- W438839775 abstract "Many studies have addressed means through which the vasculature responds to acute stress, such as changes in environmental oxygen concentration in ischemia/ reperfusion injury and exposure to toxic bacterial products, while elucidation of mechanisms underlying chronic vascular dysfunction has been more difficult. Although more sustained changes in vascular properties could simply reflect the persistent action of mediators associated with the acute vascular response, such as elaboration of cytokines, there are also likely to be factors related to the chronic disease process which drive pathogenicity. Our current concept of atherogenesis provides an example of this viewpoint [1]. Accumulation of modified lipoproteins in the vessel wall leads to activation of vascular cells, especially endothelium and smooth muscle, causing them to recruit mononuclear phagocytes and lymphocytes to a lesional site which becomes a chronic inflammatory focus W. This view suggests the relevance of a two-hit model underlying such chronic vascular processes in which an underlying perturbant, such as modified lipoproteins, provides a first hit which then perpetuates an exaggerated host response to subsequent environmental challenges." @default.
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- W438839775 date "2001-01-01" @default.
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- W438839775 title "Chronic neuronal perturbation mediated by RAGE, a receptor for β-sheet fibrils and S100/calgranulins" @default.
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