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The connection between C-reactive protein and atherosclerosis
Sanjay K Singh1, Madathilparambil V Suresh, Bhavya Voleti
1Department of Pharmacology, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37614, USA.
Insights
C-reactive protein (CRP) levels correlate with cardiovascular disease. While research shows mixed results on whether CRP is atherogenic or atheroprotective, its role in human atherosclerosis remains unclear.
Area of Science:
- Cardiovascular Science
- Immunology
- Biochemistry
Background:
- High-sensitivity C-reactive protein (hs-CRP) serum concentrations correlate with cardiovascular disease risk.
- C-reactive protein (CRP) interacts with modified and native low-density lipoprotein (LDL), and is found at atherosclerotic lesions.
- CRP's cellular effects are under re-evaluation with purified CRP preparations, free of contaminants.
Purpose of the Study:
- To investigate the multifaceted role of C-reactive protein (CRP) in the development of atherosclerosis.
- To explore the proatherogenic and atheroprotective functions of CRP in experimental models.
Main Methods:
- Correlation analysis of hs-CRP serum levels with cardiovascular disease incidence.
- In vitro studies on mammalian cell responses to CRP treatment.
- In vivo studies using experimental rats and a murine model (Apob(100/100) Ldlr(-/-)) of atherosclerosis, assessing CRP's effects on infarct size and atheroprotection.
Main Results:
- CRP concentration is linked to cardiovascular disease occurrence.
- Experimental models show conflicting results: CRP increased infarct size in rats but was atheroprotective in a murine model.
- CRP's interaction with LDL and complement activation pathways influences its effects.
Conclusions:
- CRP exhibits complex and context-dependent roles in atherosclerosis.
- Further research is needed to definitively determine if CRP protects humans against atherosclerosis.
Abstract:
The connection between C-reactive protein (CRP) and atherosclerosis lies on three grounds. First, the concentration of CRP in the serum, which is measured by using highly sensitive (a.k.a. 'hs') techniques, correlates with the occurrence of cardiovascular disease. Second, although CRP binds only to Fcgamma receptor-bearing cells and, in general, to apoptotic and damaged cells, almost every type of cultured mammalian cells has been shown to respond to CRP treatment. Many of these responses indicate proatherogenic functions of CRP but are being reinvestigated using CRP preparations that are free of endotoxins, sodium azide, and biologically active peptides derived from the protein itself. Third, CRP binds to modified forms of low-density lipoprotein (LDL), and, when aggregated, CRP can bind to native LDL as well. Accordingly, CRP is seen with LDL and damaged cells at the atherosclerotic lesions and myocardial infarcts. In experimental rats, human CRP was found to increase the infarct size, an effect that could be abrogated by blocking CRP-mediated complement activation. In the Apob (100/100) Ldlr (-/-) murine model of atherosclerosis, human CRP was shown to be atheroprotective, and the importance of CRP-LDL interactions in this protection was noted. Despite all this, at the end, the question whether CRP can protect humans from developing atherosclerosis remains unanswered.
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