Evaluating CRP and miR-29c together (AUC=0.900, p< 0.001) achieved a better prognostic value for atherosclerosis than miR-29c (AUC=0.870, p< 0.001) or CRP (AUC=0.722, p< 0.001) alone.
Overall, the oxidation of native CRP by HOCl seems to represent an alternative mechanism of CRP modification, by which CRP reveals its pro-inflammatory and pro-thrombotic properties, and as such, it might be of causal relevance in the pathogenesis of atherosclerosis.
Usefulness of Lipoprotein-Associated Phospholipase A<sub>2</sub> Activity and C-Reactive Protein in Identifying High-Risk Smokers for Atherosclerotic Cardiovascular Disease (from the Atherosclerosis Risk in Communities Study).
Increased level of VEGF and decreased level of C-reactive protein, a biological marker that is closely related to atherosclerosis, were also observed from animals treated with the bilayered NPs, implicating ameliorated atherosclerosis.
Our findings confirm the presence of premature atherosclerosis in SSc patients assessed by significant impairment of FMD, flow change and ccIMT, and it is associated with traditional cardiovascular risk factors such as age, dyslipidemia and obesity (BMI) as well as with the use of steroids and markers of inflammation such as CRP and ESR.
After adjusting for WBCC and CRP the inverse association between BRS and carotid plaque area was attenuated and did not remain significant, while both WBCC and CRP remained significantly associated with carotid plaque area, indicating that low-grade inflammation can possibly link BRS to atherosclerosis.
In conclusion, this study identifies CRP as a strong C1q recruiter and complement facilitator on CC, which may be highly relevant for the development of atherosclerosis.
Additionally, circulating free IGF-1 levels and oral glucose tolerance tests (OGTT) were assessed in cohort 1 whereas C-reactive protein levels and degree of atherosclerosis and hepatic steatosis were studied in cohort 2.
Further study elucidated that apoA-I could down-regulate the expression of some inflammatory mediators including intercellular adhesion molecule type 1, vascular adhesion molecule-1 (VCAM-1), monocyte chemoattractant protein-1, tumor necrosis factor-α, interleukin-6 (IL-6), and C-reactive protein in serum and aorta of AS rabbits.
Low-grade inflammation, represented by minor C-reactive protein (CRP) elevation, has a critical role in the early stages of atherosclerosis, and pantothenic acid (PA) may have an antioxidant effect in inflammatory process.
We evaluated baseline cross-sectional associations between smoking parameters and inflammation (high-sensitivity C-reactive protein [hsCRP]) and measures of subclinical atherosclerosis (carotid intima-media thickness, ankle-brachial index, and coronary artery calcium [CAC]).
Linear and logistic regression examined the relation between midlife high-sensitivity C-reactive protein (CRP)-a nonspecific marker of inflammation-and brain magnetic resonance imaging markers assessed 21 years later in the Atherosclerosis Risk in Communities Study.
Proinflammatory cytokines, such as C-reactive protein, tumor necrosis factor alpha (TNFα), interleukins 1 and 6, that are markedly increased in RA, play a role in the acceleration of atherosclerosis as well as myocardial fibrosis development.
Patients were assessed for anthropometry, blood pressure, measures of glycemia (fasting blood glucose, glycosylated hemoglobin), lipids [total cholesterol (TC), triglycerides, high-density lipoprotein-cholesterol, low-density lipoprotein-cholesterol, lipoprotein(a)], surrogate marker of atherosclerosis (Pulse wave velocity), and marker of inflammation (high sensitivity C-reactive protein [hs-CRP]) at baseline and after the intervention period.
The association between hs-CRP, WBC, LDL, PLT, fibrinogen, creatinine, and the amount of periodontopathogenic microorganisms indicates the possibility that periodontal treatment could decrease the risk atherosclerosis.
Influence of elevated-CRP level-related polymorphisms in non-rheumatic Caucasians on the risk of subclinical atherosclerosis and cardiovascular disease in rheumatoid arthritis.
In the process of relieving atherosclerosis, apoJ can promote cholesterol and phospholipid export from macrophage-foam cells, and exhibit cytoprotective and anti-inflammatory actions by interacting with lots of known inflammatory proteins which may predict the onset of clinical cardiovascular events and may actually play a causal role in mediating atherosclerotic disease such as C-reactive protein, paraoxonase, and leptin.
This review will highlight the complex results of genomic, epidemiological, and experimental studies on CRP and will show why further studies investigating the relationship between CRP and atherosclerosis might be needed.
In hypertensive individuals, CRP levels associate with vascular stiffness, atherosclerosis and the development of end-organ damage and cardiovascular events.