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. 2011 Dec;9(6):411–418. doi: 10.1089/met.2011.0026

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Copyright 2011, Mary Ann Liebert, Inc.

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FIG. 1. — A proposed mechanism underlying plasma lipoprotein(a) [Lp(a)] level and its impact on atherogenic risk. Lp(a) is under a strong genetic regulation of the LPA locus. In addition to an apolipoprotein(a) [apo(a)] gene size polymorphism attributable to a variable number of K2 type 2 repeats, other common genetic variants in the LPA gene, as well as in some other genes, play an important role in regulating Lp(a). Also, metabolic and environmental factors together with proinflammatory conditions modulate risk factor properties of Lp(a), in particular, Lp(a) associated with small-size apo(a). Furthermore, proinflammatory oxidized phospholipids are preferentially attached to Lp(a). These alterations in Lp(a) may enhance its proatherogenic properties and lead to an increased risk for cardiovascular disease (CVD). OxPL, oxidized phospholipid; ApoB, apolipoprotein B.