Abstract
This overview briefly summarizes the cellular pathobiology of experimental atherosclerosis and is then followed by a consideration of how 3 major risk factors interact with the hypothesized pathogenetic process. First, since hemodynamics and blood flow influence the localization of atherosclerotic plaques, possible mechanisms and directions of research are considered. Secondly, the recent hypothesis relating the oxidation of LDL to several of the early processes of atherogenesis is briefly discussed in view of the fact that hyperlipidemia is a major risk factor. The possibility that subsets of LDL and lipoproteins other than LDL might be involved is also discussed. Family history is the last of the 3 contributors to atherosclerosis reviewed and some prototypes of gene abnormalities are considered. Finally, the needs and prospects of future research are summarized.
