Abstract
Background and Aims : The atherogenicity of Lp(a) has been attributed to the pro-inflammatory oxidized phospholipids (OxPLs) bound to its apolipoprotein(a) [apo(a)] moiety. While blocking these OxPL epitopes profoundly reduces the monocytic inflammatory response, a residual IL-8 inflammatory response remains. We hypothesized that besides OxPLs, additional features contribute to the atherogenicity of Lp(a).
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