Abstract
Objective. There is a strong need for biomarkers to identify patients at risk for future cardiovascular events related with progressive atherosclerotic disease. Osteoprotegerin (OPG) protects the skeleton from excessive bone resorption by binding to receptor activator of nuclear factor-κB ligand (RANKL) and preventing it from binding to its receptor, receptor activator of nuclear factor-κB. However, conflicting results have been obtained about association of serum level of OPG or RANKL with coronary artery disease (CAD). Based on their role in inflammation and matrix degradation and the fact that atherosclerotic plaque formation is an inflammatory process, we hypothesized that RANKL : OPG ratio could be a better biomarker for CAD. Methods. In this cross-sectional study, the correlation between RANKL : OPG ratio serum concentration and coronary artery calcification (CAC) in 50 patients with ischemic coronary disease has been investigated. We used ELISA method for measuring RANKL and OPG serum concentrations. Results. There was a significant correlation between RANKL : OPG serum concentration ratio and CAC in our study population (P = 0.01). Conclusion. Our results suggested that RANKL : OPG ratio concentration has a potential of being used as a marker for coronary artery disease.
Highlights
There is a considerable demand for diagnosis and treatment of the pathologic conditions that underlie sudden cardiac events such as acute coronary syndromes and sudden cardiac death
Based on their role in inflammation and matrix degradation and the fact that atherosclerotic plaque formation is an inflammatory process, we hypothesized that RANKL : OPG ratio could be a better biomarker for coronary artery disease (CAD)
Our results suggested that RANKL : OPG ratio concentration has a potential of being used as a marker for coronary artery disease
Summary
There is a considerable demand for diagnosis and treatment of the pathologic conditions that underlie sudden cardiac events such as acute coronary syndromes and sudden cardiac death. Several retrospective autopsy series and a few cross-sectional clinical studies have suggested that thrombotic coronary death and acute coronary syndromes are caused by the plaque features [5, 6]. This phenomenon is a regular and organized process that is so similar to osteoproduction [7]. Some of the smooth muscle cells along the migration from layer to vascular media layer go osteogenic [8] These cells continuously express osteoproteins such as RANKL and OPG [4] and start to store the collagenic extracellular matrix in mineralized collections that cause vascular calcification [9].
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