Cardiovascular disease has placed a huge burden on public health systems and continues to do so, in spite of a dramatic decrease in this burden since the 1950s. It is a complex disease with numerous risk factors and a complex pathogenesis. The primary risk factor is hypercholesterolemia, which is readily influenced by dietary intakes of fats. While fats supply the substrate for atherosclerosis, it is clear that additional factors are essential for the development of plaque and ultimately the precipitation of cardiovascular disease events. Oxidation and inflammation may be the primary mechanisms for initiation and progression of atherosclerosis. Oxidative damage is associated with several CVD risk factors and could initiate vessel damage, which in turn, could induce inflammation and numerous cellular activities of atherogenesis. A primary mediator of these activities may be oxidized lipids. Oxidized lipids are formed readily in a prooxidative environment and consist of a wide variety of molecular species. Many of these species have been found in atherosclerotic plaque. In addition, several mechanisms have been identified for the regulation of reactive oxygen species and formation of oxidized lipids. Recent efforts have found that the oxidized lipids have potent biological activities. Interactions of oxidized lipids with receptors and signaling pathways have been defined and linked with the regulation of cell proliferation and apoptosis. The balance between these activities may have a significant impact on plaque development. A key regulatory factor may be mitochondria and its interaction with various redox cell signaling pathways. Mitochondria may participate in several pathways involving the formation of ROS and oxidized lipids. Subtle changes in the balance of lipid oxidation products, such as may have been induced by inhibitors of cyclooxygen-ase, could have a large impact on the incidence of CVD. Understanding these mechanisms and their modulation may be of key importance for the prevention of cardiovascular disease.

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