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Figure 1 Model of bidirectional conversion of high-density lipoprotein (HDL) from anti-inflammatory (a) to proinflammatory (b), and the role of myeloperoxidase in catalyzing oxidative modification of HDL, rendering it unable to effect adenosine triphosphate-binding cassette transporter A1-mediated cholesterol transport, modified from Fogelman et al. (2). In association with these changes, apolipoprotein A-1 (apoA-1) and paraoxonase levels decrease, while proinflammatory factors such as lipid oxidation products increase.
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