Document Detail


Effect of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibition on serum matrix metalloproteinase-13 and tissue inhibitor matrix metalloproteinase-1 levels as a sign of plaque stabilization.
MedLine Citation:
PMID:  19001938     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Atherosclerotic plaques are composed of a lipid rich core, which is covered by a collagen rich fibrous cap. Rupture of the atherosclerotic plaque with superimposed thrombosis is the main cause of acute coronary syndromes, including acute myocardial infarction and unstable angina. The stability of the plaque depends on its collagen content; degradation of the collagen leads to a vulnerable plaque that is prone to rupture. Recent studies have demonstrated a critical role for matrix metalloproteinases (MMPs) in the degradation of the collagen content and the reduction of mechanical stability of the atherosclerotic plaques. Increased expression of various MMPs has been shown in the tissue sections of atherosclerotic plaques. The increased expression of MMPs in the atheroma also leads to increased MMP levels in the circulation. The cholesterol lowering drugs - 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) - decrease the tissue expression of various MMPs in atheromatous plaques by attenuating the inflammatory process that promotes MMP expression during the course of atherosclerosis. However, the effect of statin treatment on the serum levels of MMP-13, which has a critical role in the initiation of collagen degradation, is unknown. On the basis of these previous studies, we discuss the need for studies on the effect of statin treatment on the serum levels of MMP-13 and tissue inhibitor of matrix metalloproteinase (TIMP-1) levels in hypercholesterolemic patients.
Authors:
Cihan Cevik; Mohammad Otahbachi; Kenneth Nugent; Chokesuwattanaskul Warangkana; Gary Meyerrose
Related Documents :
16777428 - Effect of recombinant human tissue inhibitor of matrix metalloproteinase-1 in rabbit ma...
15583828 - Expression of matrix metalloproteinase 9 and its regulators in the unstable coronary at...
19875168 - Mrna expression of matrix metalloproteinases (mmps) 2 and 9 and tissue inhibitor of mat...
10620188 - Nitric oxide modulates expression of matrix metalloproteinase-9 in rat mesangial cells.
23543108 - A threshold level of oxalate oxidase transgene expression reduces cryphonectria parasit...
12902548 - Molecular mechanisms of reduced beta-adrenergic signaling in the aged heart as revealed...
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Journal of cardiovascular medicine (Hagerstown, Md.)     Volume:  9     ISSN:  1558-2027     ISO Abbreviation:  J Cardiovasc Med (Hagerstown)     Publication Date:  2008 Dec 
Date Detail:
Created Date:  2008-11-12     Completed Date:  2009-02-06     Revised Date:  2009-05-28    
Medline Journal Info:
Nlm Unique ID:  101259752     Medline TA:  J Cardiovasc Med (Hagerstown)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1274-8     Citation Subset:  IM    
Affiliation:
Texas Tech University Health Sciences Center, Internal Medicine Department, Lubbock, Texas 79430, USA. cihan.cevik@ttuhsc.edu
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Anticholesteremic Agents / pharmacology*
Atherosclerosis / blood,  drug therapy
C-Reactive Protein / analysis
Humans
Hydroxymethylglutaryl-CoA Reductase Inhibitors / pharmacology*
Hypercholesterolemia / blood,  drug therapy
Matrix Metalloproteinase 13 / blood*
Tissue Inhibitor of Metalloproteinase-1 / blood*
Chemical
Reg. No./Substance:
0/Anticholesteremic Agents; 0/Hydroxymethylglutaryl-CoA Reductase Inhibitors; 0/Tissue Inhibitor of Metalloproteinase-1; 9007-41-4/C-Reactive Protein; EC 3.4.24.-/Matrix Metalloproteinase 13

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


Previous Document:  Extrusion of the device: a rare complication of the pacemaker implantation.
Next Document:  Use of electroanatomic mapping in the assessment of atrial tachycardia aetiology.