Abstract
High levels of lipoprotein (a) [Lp(a)] are an independent risk factor for a number of cardiovascular diseases such coronary heart disease, stroke and restenosis. In addition, numerous clinical and experimental studies indicate that Lp(a), similar to LDL, is an atherogenic lipoprotein, and thus, increased plasma concentrations of Lp(a) may be associated with premature atherosclerosis. Despite the progress in these studies during the past years, the precise physiological functions of Lp(a) is still unknown, and its pathological roles on the pathogenesis of atherosclerosis have not been fully defined. To investigate the functional roles of Lp(a), our laboratory has generated transgenic rabbits expressing human apolipoprotein (a) [apo(a)], and recently, we demonstrated that Lp(a) enhances diet-induced atherosclerosis and vascular calcification in transgenic rabbits. In this article, we summarize the progress in the study of human apo(a) transgenic rabbits.
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