The response-to-retention hypothesis of early atherogenesis

KJ Williams, I Tabas - Arteriosclerosis, thrombosis, and vascular …, 1995 - Am Heart Assoc
Arteriosclerosis, thrombosis, and vascular biology, 1995Am Heart Assoc
M any processes have been implicated in early atherogenesis. These include endothelial
denudation, injury, or activation, including shear stress-related events; local adherence of
platelets; lipoprotein oxidation; lipoprotein aggregation; macrophage chemotaxis and foam
cell formation; and smooth muscle cell alterations. Which process, if any, could be regarded
as the key event in early atherogenesis, ie, absolutely required, yet also sufficient as the sole
pathological stimulus in an otherwise normal artery to provoke a cascade of events leading …
M any processes have been implicated in early atherogenesis. These include endothelial denudation, injury, or activation, including shear stress-related events; local adherence of platelets; lipoprotein oxidation; lipoprotein aggregation; macrophage chemotaxis and foam cell formation; and smooth muscle cell alterations. Which process, if any, could be regarded as the key event in early atherogenesis, ie, absolutely required, yet also sufficient as the sole pathological stimulus in an otherwise normal artery to provoke a cascade of events leading to lesion formation? The work of many investigators, which we summarize here, strongly supports subendothelial retention of atherogenic lipoproteins as the central pathogenic process in atherogenesis (for prior reviews, see References 1 through 6). Our thesis is that other contributory processes are either not individually necessary or are not sufficient. Most often, they are merely normal, expected responses of otherwise-healthy tissue to the presence of retained lipoproteins.
Am Heart Assoc