Abstract
High-density lipoprotein (HDL) protects against atherosclerosis, transporting cholesterol from peripheral cells to the liver, where it is excreted into the bile. However, HDL also has prominent vascular protective effects. Recent studies have uncovered mechanisms through which HDL decreases vascular inflammation, boosts nitric oxide production, and inhibits thrombosis. The discovery that dysfunctional HDL can also have proinflammatory effects has uncovered a new aspect of HDL biology. Low-density lipoprotein is the primary target for drug therapy of dyslipidemias. Drugs that increase HDL also affect additional metabolic pathways. Development of selective drugs targeting key aspects of HDL metabolism may enable us to alter the composition of HDL and inhibit atherogenesis.
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