Key result
Elevated CRP tracks with cardiovascular disease, but apparent causal proatherogenic effects may reflect contaminated preparations.
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Atherosclerosis is considered a to be multifactorial disease driven by inflammatory reactions. The process of inflammation also contributes to the pathogenesis of acute atherothrombotic events. C-reactive protein (CRP) is an acute phase protein and its concentration in serum reflects the inflammatory condition of the patient. Levels of CRP are consistently associated with cardiovascular disease (CVD) and predict myocardial infarctions and stroke. Since CRP is present in the atherosclerotic lesion, it may actively contribute to the progression and/or instability of the atherosclerotic plaque. The role of CRP in inflammation and its causality in atherosclerosis are the subject of many investigations but are not yet fully elucidated. This review focuses on recently identified mechanisms by which CRP may modulate and evolve the process of atherosclerosis. We discuss the function of CRP and review the most recent evidence for an independent role of CRP in the development of atherosclerosis. Many studies suggest such a role, but a number of the described effects may be the result of contamination of the CRP preparations.
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Paffen et al. (2006) conducted a review in Atherosclerosis and cardiovascular disease. C-reactive protein (CRP) was evaluated on Development and progression of atherosclerosis. C-reactive protein levels are consistently associated with cardiovascular disease, though apparent causal effects on atherosclerosis may result from contaminated CRP preparations.
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