Lipoprotein(a) exhibits antifibrinolytic and procoagulant properties, impacting platelet function through mechanisms potentially involving both its LDL-like lipid moiety and apo(a) components.
Plasma levels of lipoprotein(a), Lp(a), is an independent risk factor for cardiovascular disease. Lp(a) has many properties in common with low-density lipoprotein (LDL), including a cholesteryl ester-rich lipid core and the presence of one copy of apolipoprotein B-100; both apoB-100 and the lipid core are pro-atherogenic. In addition, Lp(a) contains a unique hydrophilic, carbohydrate-rich protein, apo(a), linked to apoB through a single disulfide bond connecting the C-terminal regions of the two proteins. The similarities between apolipoprotein(a), apo(a), and plasminogen has initiated numerous studies on the possible role of Lp(a) as a prothrombotic agent. Studies to date suggest that Lp(a) has antifibrinolytic and procoagulant properties. In this review, we summarize recent studies focused on the interaction between Lp(a) and platelets. Collectively, results to date illustrate that thrombogenicity associated with Lp(a) could be due to risk associated with the LDL moiety, with the apo(a) moiety, or from the combination of those in Lp(a). Present findings suggest that the various components of Lp(a) may impact to a varying degree on different underlying pathways involved in platelet activation and aggregation. On balance, results indicate an effect by Lp(a) on platelet function and future studies focused on specific Lp(a) components, such as the role of apo(a) and of the LDL-like lipid moiety, are needed.
Discepolo et al. (Sun,) conducted a review in Cardiovascular disease. Lipoprotein(a) was evaluated. Lipoprotein(a) exhibits antifibrinolytic and procoagulant properties, impacting platelet function through mechanisms potentially involving both its LDL-like lipid moiety and apo(a) components.