“…Interestingly, established lesions contain oxidized lipids that have lost their stereospecificity, indicating non-enzymatic lipid peroxidation occurs later in atherosclerosis progression (Kuhn et al, 1994(Kuhn et al, , 1997. Following from this work, several groups examined mechanisms and consequences of free and cell-expressed LOX oxidation of LDL, and found that this process formed a high-uptake LDL form, similar to that found in atherosclerotic lesions, and that this requires LDL receptor related protein, and can be enhanced by angiotensin II, lipoprotein lipase and secretory phospholipase A 2 (Scheidegger et al, 1997;Sigari et al, 1997;Belkner et al, 1998;Neuzil et al, 1998;Xu et al, 2003;Zhu et al, 2003).…”