Increasing evidence has highlighted the roles of oxidative stress and inflammation in the promotion of atherosclerotic cardiovascular disease. Recent pathological studies have elucidated specific mediators that appear to link these pathways to the progression and rupture of atherosclerotic plaque in the artery wall. The ability to measure levels of these mediators in the systemic circulation has provoked interest in their development as biomarkers for potential use in risk assessment and in evaluation of the response to the use of preventive therapies. The discovery of these pathological mediators and their potential translation to the clinical arena will be reviewed.
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Uno et al. (2010) studied this question.
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