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Updated: Aug 9, 2026

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
Published on: May 6, 2014
C-reactive protein in atherosclerosis: A causal factor?
Elaine Paffen1, Moniek P M DeMaat
1Hemostasis and Thrombosis Research Centre, Dept. of Hematology, Leiden University Medical Centre, Leiden, The Netherlands.
Insights
C-reactive protein (CRP) is linked to cardiovascular disease and may drive atherosclerosis progression. Further research is needed to clarify CRP's exact role in inflammation and plaque development.
Area of Science:
- Cardiovascular Science
- Immunology
- Biochemistry
Background:
- Atherosclerosis is a multifactorial inflammatory disease.
- C-reactive protein (CRP) indicates systemic inflammation and predicts cardiovascular events.
- CRP presence in atherosclerotic lesions suggests a potential role in plaque progression.
Purpose of the Study:
- To review recent mechanisms of C-reactive protein (CRP) in atherosclerosis.
- To discuss the function of CRP in inflammation.
- To evaluate evidence for CRP's independent role in atherosclerosis development.
Main Methods:
- Literature review of recent studies on CRP and atherosclerosis.
- Analysis of CRP's function in inflammatory pathways.
- Examination of evidence for CRP's direct contribution to atherosclerotic plaque.
Main Results:
- CRP concentration reflects a patient's inflammatory state.
- CRP is associated with cardiovascular disease (CVD), myocardial infarction, and stroke.
- Recent evidence suggests CRP may actively contribute to atherosclerotic plaque progression and instability.
Conclusions:
- CRP's precise role in atherosclerosis pathogenesis requires further elucidation.
- Potential mechanisms link CRP to inflammation and atherosclerotic plaque evolution.
- Contamination in CRP preparations may affect study outcomes.
Abstract:
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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