title: Therapeutic interventions targeted at the augmentation of reverse cholesterol transport.
abstract: OBJECTIVE
  Serum high-density lipoproteins (HDLs) and reverse cholesterol transport (RCT) are important therapeutic targets in the management of atherosclerotic disease. This review summarizes the pathway of RCT and the currently available means by which investigators are attempting to modulate HDL levels and increase rates of RCT.
  
  
  RESULTS
  Low levels of HDL are commonly encountered in patients with atherosclerotic disease. HDLs mediate a substantial number of antiatherogenic effects along blood vessel walls. One of the most important of these antiatherogenic mechanisms is RCT, a series of reactions by which HDL is able to facilitate the net translocation of cholesterol from peripheral cells to the liver for excretion. There is scientific evidence supporting the concept of RCT in both animals and humans. To facilitate RCT, it is important that therapeutic effort be made to raise serum levels of HDL. Statins, fibrates, niacin, thiazolidinediones, and various combinations of these drugs all raise HDL levels. However, in many high-risk patients with established atherosclerotic disease, the elevations in HDL achieved with these medications are frequently inadequate. Newer agents designed to raise HDL and promote RCT are currently being developed, including infusible bioengineered HDL, edible HDL composed of D-amino acids, and agents capable of inhibiting cholesterol ester transfer protein, among others.
  
  
  CONCLUSIONS
  Established therapies for raising HDL can be effective either as monotherapy or when used in combination. Newer strategies are being developed to exploit more specifically the capacity of HDL to drive RCT and either prevent or reverse the course of atherosclerotic disease.
authors.affiliation: Sterling Rock Falls Clinic, Sterling, Illinois 61081, USA. peter.toth@srfc.com
authors.forename: Peter P
authors.initials: PP
authors.lastname: Toth
authors.forename: Michael H
authors.initials: MH
authors.lastname: Davidson
mesh_terms: D016632:Apolipoprotein A-I / Q000378:metabolism; D001161:Arteriosclerosis / Q000188:drug therapy*; D001693:Biological Transport, Active / Q000187:drug effects; D002352:Carrier Proteins / Q000378:metabolism; D002784:Cholesterol / Q000378:metabolism*; D053480:Cholesterol Ester Transfer Proteins; D006023:Glycoproteins / Q000378:metabolism; D006801:Humans; D000960:Hypolipidemic Agents / Q000494:pharmacology* / Q000627:therapeutic use; D008049:Lipase / Q000378:metabolism; D008071:Lipoprotein Lipase / Q000378:metabolism; D008075:Lipoproteins, HDL / Q000097:blood / Q000187:drug effects* / Q000502:physiology
chemical_list: C108069:ATP-binding protein, liver; D016632:Apolipoprotein A-I; C506642:CETP protein, human; D002352:Carrier Proteins; D053480:Cholesterol Ester Transfer Proteins; D006023:Glycoproteins; D000960:Hypolipidemic Agents; C504173:LIPC protein, human; D008075:Lipoproteins, HDL; D002784:Cholesterol; D008049:Lipase; D008071:Lipoprotein Lipase