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Published on: August 5, 2012
C-reactive protein is a mediator of cardiovascular disease
Radjesh J Bisoendial1, S Matthijs Boekholdt, Menno Vergeer
1Department of Vascular Medicine, Academic Medical Center, PO Box 22660, 1100 DD Amsterdam, The Netherlands.
Insights
C-reactive protein (CRP) is a marker for cardiovascular risk and a key player in atherosclerosis development. Targeting CRP may offer new strategies for preventing cardiovascular disease.
Area of Science:
- Biochemistry
- Cardiology
- Immunology
Background:
- C-reactive protein (CRP) has been recognized as a predictor of cardiovascular events and mortality.
- Emerging evidence shows CRP is present in atherosclerotic lesions and initiates pathogenic pathways.
- This suggests CRP is actively involved in atherosclerosis, not just an indicator.
Purpose of the Study:
- To review the evolving understanding of C-reactive protein's role in cardiovascular disease.
- To highlight the shift from CRP as a risk marker to a pathogenic factor.
- To emphasize the potential of targeting CRP for therapeutic interventions.
Main Methods:
- Literature review of experimental data on CRP in atherosclerosis.
- Analysis of studies investigating CRP's role in atherogenic pathways.
- Synthesis of evidence supporting CRP's involvement in disease pathogenesis.
Main Results:
- C-reactive protein is abundant in atherosclerotic lesions.
- CRP initiates key pathogenic pathways contributing to atherogenesis.
- Data support CRP's direct role in the development of cardiovascular disease.
Conclusions:
- C-reactive protein is a direct participant in atherosclerotic cardiovascular disease pathogenesis.
- The paradigm has shifted, viewing CRP as more than just a risk indicator.
- Inhibiting CRP activity presents a novel therapeutic strategy for atherosclerosis prevention.
Abstract:
C-reactive protein is postulated to embody an index that can reflect cardiovascular risk and can be used to independently predict major cardiovascular events and mortality. On the other hand, credible experimental data have become available that demonstrate the abundant presence of C-reactive protein in atherosclerotic lesions and, moreover, identify C-reactive protein as an initiator of several pathogenic pathways that can cause atherogenic changes. Consequently, there has been a paradigm shift in which C-reactive protein is no longer regarded as merely an indicator of cardiovascular risk, but increasingly considered a direct partaker in the pathogenesis of atherosclerotic cardiovascular disease. These data underscore the need to explore risk-reducing interventions that selectively inhibit C-reactive protein activity as a novel strategy to prevent clinical manifestations of atherosclerosis.
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