Abstract
The current study demonstrates that a disintegrin and metalloproteinase with thrombospondin type 1 motif- (ADAMTS-) 5 is a key extracellular matrix protease and associated with cardiovascular diseases. However, the plasma ADAMTS-5 levels and relevance of coronary artery disease (CAD) remain largely unknown. This study is aimed at examining the relationship between the plasma ADAMTS-5 levels and the severity of coronary stenosis in patients with CAD. In the present study, the expression of ADAMTS-5 was analyzed in coronary artery samples and blood. The results showed that the plasma ADAMTS-5 levels were lower in the CAD group than in the control group. In addition, significantly higher matrix metalloproteinase- (MMP-) 2 and MMP-9 levels were also observed in the patients with CAD, and the ADAMTS-5 levels were negatively correlated with the MMP-2 and MMP-9 levels. Spearman's correlation analysis showed that the Gensini score was negatively correlated with the ADAMTS-5 levels but was positively correlated with the MMP-2 and MMP-9 levels. Receiver-operating characteristic (ROC) analysis revealed that ADAMTS-5, MMP-2, and MMP-9 may have a certain diagnostic value in CAD and that the combination of all three metalloproteinases had a higher diagnostic value. The findings provided a better understanding of the role of ADAMTS-5 in the diagnosis of CAD.
Highlights
Coronary atherosclerotic disease (CAD) is the most common cardiovascular disease and remains a leading cause of morbidity and mortality worldwide
No differences were found between normal donors and patients with CAD for other clinical characteristics, including gender, age, smoking, glucose (Glu), total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), systolic blood pressure (SBP), and diastolic blood pressure (DBP)
To investigate the potential role of ADAM with thrombospondin type motif (ADAMTS)-5 in the progression of CAD, we examined whether ADAMTS-5 expression levels were altered in atheromatous plaques
Summary
Coronary atherosclerotic disease (CAD) is the most common cardiovascular disease and remains a leading cause of morbidity and mortality worldwide. Narrowing of the arterial lumen and rupture of coronary atherosclerotic plaques with or without luminal thrombosis and vasospasm are currently considered to be the main causes of CAD [1,2,3,4,5]. The ECM is the most abundant component of normal vessels and atherosclerotic plaque, including fibrous caps. Plaque rupture is increased by a weakened fibrous cap, promoted by the loss of function of the vascular smooth muscle cells (VSMCs) and the breakdown of collagen and ECM that may subsequently lead to acute myocardial infarction (AMI) or stroke [9, 10]
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