Biomarkers Associated with Vulnerable Atheromatous Plaque

Author(s): Toshio Imanishi, Takashi Akasaka.

Journal Name: Current Medicinal Chemistry

Volume 19 , Issue 16 , 2012

Become EABM
Become Reviewer

Abstract:

Atherogenesis progresses through lipid core expansion and macrophage accumulation at the plaque, leading to fibrous cap rupture. Plaque rupture occurs in the plaque fissuring at one point, which ultimately brings the platelets into contact with the content of the lipid core, and the blood coagulation factors together with tissue factor. The transition from stable atherosclerotic plaques to vulnerable plaques finally resulting in the plaque rupture is the consequence of an inflammatory reaction. This process involves complex cellular interactions engaging many mediators, chemokines, and cytokines which can be measured in serum and plasma and thus serve as biomarkers that differentiate the pathophysiologic phases of disease progression. Pathological studies support the risk of inflammation in high-risk patients to a greater extent than the degree of vessel stenosis. It is therefore important to identify reliable biomarkers allowing us to monitor vascular inflammatory state.

In clinical investigations, several new biomarkers have been identified that provide increasing diagnostic and prognostic significance. However, more confirmatory studies are required to clinical use. Furthermore, assays for automated use need to be developed, and cut-off levels need to be defined. Further technological advances will likely facilitate the use of multimarker profiling to identify with coronary vulnerable plaque.

Keywords: Atherosclerosis, Biomarkers, Vulnerable Plaque, Inflammattion, Chemokines, Cytokines, Oxidative Stress, macrophage accumulation, inflammatory reaction, cytokines

Rights & PermissionsPrintExport Cite as

Article Details

VOLUME: 19
ISSUE: 16
Year: 2012
Page: [2588 - 2596]
Pages: 9
DOI: 10.2174/092986712800492922
Price: $58

Article Metrics

PDF: 14