Cholesterol efflux and HDL function

linked to atherosclerosis. Knowledge about HDL metabolism is necessary to use this relationship as a therapeutic approach to address atherosclerosis. Different proteins are involved in HDL metabolism and include structural proteins, such as apolipoprotein A1(apoA1), apoA2 and apoE, enzymes or transport proteins, such as lecithin- cholesterol acyltransferase (LCAT) or cholesteryl ester transfer protein (CETP) and cellular transporters, such as ATP-binding cassette transporter A1 (ABCA1), ATP-binding cassette transporter G1 (ABCG1) and scavenger receptor B1 (SR-B1). These components are necessary to warrant cholesterol efflux and also for the anti-inflammatory, antioxi-dative and antithrombotic properties of HDL. Because of the complexity of HDL metabolism it is difficult to predict whether interventions affecting HDL levels or function will be proatherogenic, antiatherogenic or neutral. However, the epidemiological as well as the genetic data indicate that modulations of the HDL system will influence atherosclerosis. Therefore, HDL modifying interventions are an interesting approach to address residual risks associated with statin therapy.