Document Detail


Macrophage cholesterol homeostasis and metabolic diseases: critical role of cholesteryl ester mobilization.
MedLine Citation:
PMID:  21438812     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Atherogenic dyslipidemia, including low HDL levels, is the major contributor of residual risk of cardiovascular disease that remains even after aggressive statin therapy to reduce LDL-cholesterol. Currently, distinction is not made between HDL-cholesterol and HDL, which is a lipoprotein consisting of several proteins and a core containing cholesteryl esters (CEs). The importance of assessing HDL functionality, specifically its role in facilitating cholesterol efflux from foam cells, is relevant to atherogenesis. Since HDLs can only remove unesterified cholesterol from macrophages while cholesterol is stored as CEs within foam cells, intracellular CE hydrolysis by CE hydrolase is vital. Reduction in macrophage lipid burden not only attenuates atherosclerosis but also reduces inflammation and linked pathologies such as Type 2 diabetes and chronic kidney disease. Targeting reduction in macrophage CE levels and focusing on enhancing cholesterol flux from peripheral tissues to liver for final elimination is proposed.
Authors:
Shobha Ghosh
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Expert review of cardiovascular therapy     Volume:  9     ISSN:  1744-8344     ISO Abbreviation:  Expert Rev Cardiovasc Ther     Publication Date:  2011 Mar 
Date Detail:
Created Date:  2011-03-28     Completed Date:  2011-07-26     Revised Date:  2013-05-24    
Medline Journal Info:
Nlm Unique ID:  101182328     Medline TA:  Expert Rev Cardiovasc Ther     Country:  England    
Other Details:
Languages:  eng     Pagination:  329-40     Citation Subset:  IM    
Affiliation:
Department of Internal Medicine, Division of Pulmonary and Critical Care, VCU Medical Center, Richmond, VA 23298-0050, USA. shobha@vcu.edu
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Atherosclerosis / metabolism,  physiopathology
Cholesterol / metabolism*
Cholesterol Esters / metabolism*
Homeostasis
Humans
Inflammation / physiopathology
Lipid Mobilization
Lipoproteins, HDL / metabolism
Macrophages / metabolism
Metabolic Diseases / physiopathology*
Grant Support
ID/Acronym/Agency:
HL069946/HL/NHLBI NIH HHS; HL097346/HL/NHLBI NIH HHS; R01 HL069946-09/HL/NHLBI NIH HHS; R01 HL097346-03/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Cholesterol Esters; 0/Lipoproteins, HDL; 57-88-5/Cholesterol
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Hepatic steatosis and Type 2 diabetes: current and future treatment considerations.
Next Document:  Diabetic dyslipidemia or 'diabetes lipidus'?