Although several population studies have shown that plasma levels of oxidized LDL (oxLDL) are associated with cardiovascular disease (CVD), whether lowering plasma oxLDL levels slows the progression of CVD remains largely unknown. To address this issue, Ishigaki et al. sought to determine whether the removal of plasma oxLDL through the hepatic expression of lectin-like oxLDL receptor (LOX-1) would slow the progression of atherosclerosis in apolipoprotein-E deficient mice, which are prone to atherosclerosis. Although LOX-1 expression in the liver led to the removal of plasma oxLDL levels, they found no apparent changes in plasma levels of plasma cholesterol or triglycerides. Interestingly, 4 weeks after the adenoviral administration, atherosclerosis lesions decreased by 38%. In addition, plasma levels of monocyte chemoattractant protein-1 and lipid peroxide levels decreased and plasma adiponectin levels increased, suggesting a decrease in systemic inflammation and oxidative stress. Since these results suggest that removal of plasma oxLDL is likely to slow foam cell formation, pharmacotherapy aimed at lowering plasma oxLDL levels could not only slow atherosclerosis but also reduce the risk of acute coronary syndromes in high-risk patients.
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