Biomarkers of atherosclerotic plaque instability and rupture

TY - JOUR

T1 - Biomarkers of atherosclerotic plaque instability and rupture

AU - Koenig, Wolfgang

AU - Khuseyinova, Natalie

PY - 2007/1

Y1 - 2007/1

N2 - Basic research over the last two decades has identified a large number of molecules pertinent to the atherosclerotic process, which have clearly improved our understanding of the underlying pathology. It is now well established that inflammation represents a major feature which is present in the vessel wall throughout all stages of the disease until the final pathophysiologic steps, representing plaque destabilization and eventually plaque rupture. Several cells typical for the atherosclerotic plaque, like monocyte-derived macrophages and T-lymphocytes are able to produce and secrete such mediator molecules, like cytokines, chemokines, growth-factors, enzymes, and disintegrins, which lead to activation of endothelial cells, proliferation of smooth muscle cells, lesion progression, and finally to the weakening of a vulnerable plaque by matrix degradation of its fibrous cap. Today, many of these molecules involved can be measured systemically by sensitive assays, and elevated concentrations in the circulation have been shown to be associated with future cardiovascular events. Determination of several of these molecules carries important prognostic information, independent of traditional risk factors, and may turn out to be useful in improving risk stratification. However, for most of these biomarkers the clinical utility has not yet been established.

AB - Basic research over the last two decades has identified a large number of molecules pertinent to the atherosclerotic process, which have clearly improved our understanding of the underlying pathology. It is now well established that inflammation represents a major feature which is present in the vessel wall throughout all stages of the disease until the final pathophysiologic steps, representing plaque destabilization and eventually plaque rupture. Several cells typical for the atherosclerotic plaque, like monocyte-derived macrophages and T-lymphocytes are able to produce and secrete such mediator molecules, like cytokines, chemokines, growth-factors, enzymes, and disintegrins, which lead to activation of endothelial cells, proliferation of smooth muscle cells, lesion progression, and finally to the weakening of a vulnerable plaque by matrix degradation of its fibrous cap. Today, many of these molecules involved can be measured systemically by sensitive assays, and elevated concentrations in the circulation have been shown to be associated with future cardiovascular events. Determination of several of these molecules carries important prognostic information, independent of traditional risk factors, and may turn out to be useful in improving risk stratification. However, for most of these biomarkers the clinical utility has not yet been established.

KW - Animals

KW - Atherosclerosis/metabolism

KW - Biomarkers/metabolism

KW - C-Reactive Protein/metabolism

KW - Carotid Stenosis/metabolism

KW - Chemokines/metabolism

KW - Cytokines/metabolism

KW - Disintegrins/metabolism

KW - Humans

KW - Intercellular Signaling Peptides and Proteins/metabolism

KW - Risk Factors

KW - Rupture, Spontaneous/metabolism

U2 - 10.1161/01.ATV.0000251503.35795.4f

DO - 10.1161/01.ATV.0000251503.35795.4f

M3 - SCORING: Review article

C2 - 17082488

VL - 27

SP - 15

EP - 26

JO - ARTERIOSCL THROM VAS

JF - ARTERIOSCL THROM VAS

SN - 1079-5642

IS - 1

ER -