title: The controversy over the use of cholesteryl ester transfer protein inhibitors: is there some light at the end of the tunnel?
abstract: BACKGROUND
  According to epidemiological studies, there is no clear relationship between the plasma cholesteryl ester transfer protein (CETP) concentration and the development of atherosclerosis in human populations. Although some studies suggest that increased CETP activity relates to undesirable profiles of plasma lipoproteins, promoting an anti-atherogenic plasma lipoprotein profile by drugs that inhibit CETP has not succeeded in preventing atherosclerosis in humans.
  
  
  METHODS
  This review describes 28 investigations in human populations dealing with plasma CETP, 11 in mice that express human CETP and seven in animals (six in rabbits and one in mice) in which plasma CETP activity was inhibited by drugs.
  
  
  RESULTS
  Present review shows that models in mice expressing human CETP are not illuminating because they report increase as well reduction of atherosclerosis. However, investigations in rabbits and mice that develop severe hypercholesterolaemia clearly indicate that impairment of the plasma CETP activity elicits protection against the development of atherosclerosis; in all of these experiments are attained substantial reductions of the atherogenic lipoproteins, namely, plasma apoB containing lipoproteins.
  
  
  CONCLUSIONS
  These models are strong indicators that the benefit in preventing atherosclerosis should be earned in cases of hyperlipidemia by CETP inhibitors.
authors.affiliation: Internal Medicine, University of Sao Paulo Medical School, Sao Paulo, Brazil.
authors.forename: Eder C R
authors.initials: EC
authors.lastname: Quintão
mesh_terms: D000577:Amides; D000818:Animals; D000924:Anticholesteremic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D001055:Apolipoproteins B / Q000187:drug effects / Q000378:metabolism; D050197:Atherosclerosis / Q000188:drug therapy* / Q000378:metabolism; D001569:Benzodiazepines / Q000494:pharmacology / Q000627:therapeutic use; D053480:Cholesterol Ester Transfer Proteins / Q000037:antagonists & inhibitors / Q000378:metabolism*; D004952:Esters; D006801:Humans; D006937:Hypercholesterolemia / Q000188:drug therapy* / Q000378:metabolism; D051379:Mice; D023303:Oxazolidinones / Q000494:pharmacology / Q000627:therapeutic use; D011804:Quinolines / Q000494:pharmacology / Q000627:therapeutic use; D011817:Rabbits; D013438:Sulfhydryl Compounds / Q000494:pharmacology / Q000627:therapeutic use
chemical_list: D000577:Amides; D000924:Anticholesteremic Agents; D001055:Apolipoproteins B; C506642:CETP protein, human; D053480:Cholesterol Ester Transfer Proteins; D004952:Esters; D023303:Oxazolidinones; D011804:Quinolines; D013438:Sulfhydryl Compounds; D001569:Benzodiazepines; C411602:dalcetrapib; C483909:torcetrapib; C568301:evacetrapib; C530884:anacetrapib
keywords: Atherosclerosis; cholesteryl ester transfer protein; cholesteryl ester transfer protein inhibition; high-density lipoprotein; hyperlipidemia