Oxidation of low-density lipoprotein-cholesterol (LDL-C), the major cholesterol-carrying lipoprotein in plasma, is commonly implicated as an initiator of atherosclerosis. Increased LDL-C concentration is a major risk factor for atherosclerosis in humans (Carmena et al., 2004). Oxidised LDL-C is engulfed by macrophages, a type of white blood cell, and this rapidly leads to the formation of atherosclerotic plaques. The sequential steps in the formation of foam cells (fat-laden macrophages) will eventually culminate in their rupture into fatty streaks. Over time, these fatty streaks mature into fatty plaques and accumulate in the arterial wall, reducing the size of the blood vessel lumen. This inhibits blood flow to the heart and brain and eventually blocks the artery, which may result in a heart attack or stroke (Ross, 1993, Tedgui and Mallat, 2006).