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oxidized PL/ apo B level is conversely increased. Third, oxidized LDLs in the present study are insignificantly correlated with lipoprotein(a) [Lp(a)], but oxidized PL/apo B is markedly correlated with Lp(a), which is a carrier of oxidized PL . For comparison, MDA–LDL is not correlated with Lp(a). Nevertheless, both markers of oxidatively modified LDL (the present study’s oxidized LDL and oxidized PL/ apo B) were similarly associated with carotid atherosclerosis progression. Despite intensive research on LDL oxidative modification relevant to atherogenesis, many questions remain to be delineated even now. As mentioned as a study limitation by Gao et al., whether circulating oxidized LDLs reflect the atherogenic actions of oxidized LDLs present in the atherosclerotic lesions has not been fully understood yet. Oxidized LDLs in the present study are different from oxidized PL/apo B reported by Tsimikas et al. , and thus, standardization of evaluating methods for oxidized LDL may be required. Otherwise, these issues and differences may still leave difficulty in the comparison of oxidized LDL-related clinical studies. In addition, clinical trials on antioxidants including vitamin E and beta-carotene failed to show that they prevent cardiovascular diseases. To answer all questions, further studies at a basic level and in clinical settings will provide a hopeful framework for revisiting the lipoprotein oxidation hypothesis related to atherosclerotic cardiovascular diseases.

journal of atherosclerosis and thrombosis

An Intriguing and Important Concept Relevant to Oxidized Low-Density Lipoprotein and Atherogenesis is Still Problematic for its Contribution to the Better Understanding of Clinical Atherosclerosis