Abstract
Disruption of vulnerable plaques is the main cause of acute coronary syndrome (ACS). It was reported that reactive oxygen species (ROS) activate matrix metalloproteinases. Therefore, the oxidative stress likely plays an important role in atherogenesis as well as plaque instability. Recent investigations demonstrated the presence of CRP, a potent risk factor of cardiovascular disease, in atherosclerotic vessels, and that CRP has direct pro-inflammatory effects on vascular cells such as induction of adhesion molecules and chemokines. In this review, we discuss the interaction of oxidative stress and inflammatory response in the plaque instability focusing on CRP.
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