Investigators have shown that a decrease in the release of tissue plasminogen activator (tPA) and an elevation of plasminogen activator inhibitor 1 (PAI-1) will reduce fibrinolytic function. It has emerged that triacylglycerol-rich lipoproteins stimulate PAI-1 secretion from endothelial cells, and furthermore it has been shown that OxLDL induces secretion, whereas native LDL has no detectable effect. Lipoprotein (a) (Lp(a)) has also been linked with a decrease in fibrinolysis. Lp(a) is an LDL-like particle consisting of the protein apo(a). It is believed that apo(a) competes with plasminogen and plasmin for binding to fibrin, thus interfering with fibrinolysis; LDL and Lp(a) may represent, therefore, an important link between thrombotic and lipid mechanisms in atherogenesis.
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