Document Detail


Therapeutic interventions to enhance apolipoprotein A-I-mediated cardioprotection.
MedLine Citation:
PMID:  20297868     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The principal function of high-density lipoprotein (HDL) is to facilitate the reverse cholesterol transport (RCT) and inhibition of atheroma formation. Epidemiological studies and interventional trials have suggested that HDL has cardioprotective properties. However, increasing HDL concentration may not necessarily increase RCT, especially if the increase in HDL levels is the result of inhibiting HDL cholesterol (HDL-C) flux. The results of recent phase III clinical trials utilizing a cholesterol ester transfer protein (CETP) inhibitor to increase HDL-C levels in hypoalphalipoproteinaemia have shown that this approach of elevating HDL-C levels is insufficient to combat atherosclerosis and reduce the risk of cardiovascular disease. Although there are several interventions that increase HDL-C by preventing its turnover in the circulation, a more desirable approach is to enhance de novo production of HDL in the liver and/or small intestine. To this end, our acquired knowledge of the apolipoprotein-I (apo A-I) gene promoter as well as the signalling pathways that modulate its expression, has fuelled the development of novel therapeutic strategies to increase HDL-C flux. Promising pharmacological agents that selectively regulate transcription of the apo A-I gene, therapeutic strategies to de-repress apo A-I gene expression, and infusion of recombinant apo A-I or apo A-I mimetics are under development and may be clinically beneficial in the near future.
Authors:
Michael J Haas; Arshag D Mooradian
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Drugs     Volume:  70     ISSN:  0012-6667     ISO Abbreviation:  Drugs     Publication Date:  2010 May 
Date Detail:
Created Date:  2010-04-29     Completed Date:  2010-07-16     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7600076     Medline TA:  Drugs     Country:  New Zealand    
Other Details:
Languages:  eng     Pagination:  805-21     Citation Subset:  IM    
Affiliation:
Department of Medicine, University of Florida College of Medicine, Jacksonville, Florida 32209, USA. michael.haas@jax.ufl.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Apolipoprotein A-I / biosynthesis*,  genetics
Biological Transport
Cardiotonic Agents / pharmacology,  therapeutic use*
Cardiovascular Diseases / drug therapy*,  metabolism
Cholesterol / metabolism*
Drug Design*
Humans
Lipoproteins, HDL / biosynthesis*
Promoter Regions, Genetic / drug effects
Receptors, Cytoplasmic and Nuclear / agonists,  antagonists & inhibitors
Transcription, Genetic / drug effects
Chemical
Reg. No./Substance:
0/Apolipoprotein A-I; 0/Cardiotonic Agents; 0/Lipoproteins, HDL; 0/Receptors, Cytoplasmic and Nuclear; 57-88-5/Cholesterol

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