scholarly journals Pentraxin 3: A Novel Biomarker for Inflammatory Cardiovascular Disease

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Kenji Inoue ◽  
Tatsuhiko Kodama ◽  
Hiroyuki Daida
Keyword(s):  
Gene Expression ◽  
Cardiovascular Disease ◽  
Pentraxin 3 ◽  
Human Endothelial Cells ◽  
C Reactive Protein ◽  
Physiological Concentration ◽  
Reactive Protein ◽  
Atherosclerotic Lesions ◽  
Human Genes

Numerous studies have recently examined the role of pentraxin 3 (PTX3) in clinical situations. The pentraxin family includes C-reactive protein (CRP); however, unlike CRP, PTX3 is expressed predominantly in atherosclerotic lesions that involve macrophages, neutrophils, dendritic cells, or smooth muscle cells. Interestingly, PTX3 gene expression in human endothelial cells is suppressed to a greater extent by pitavastatin than the expression of 6,000 other human genes that have been examined, suggesting that PTX3 may be a novel biomarker for inflammatory cardiovascular disease. The expression and involvement of PTX3 in cardiovascular diseases are discussed in this paper, along with the characteristics of PTX3 that make it a suitable biomarker; namely, that the physiological concentration is known and it is independent of other risk factors. The results discussed in this paper suggest that further investigations into the potential novel use of PTX3 as a biomarker for inflammatory cardiovascular disease should be undertaken.

scholarly journals C-Reactive Protein in Human Atherogenesis: Facts and Fiction

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Oliver Zimmermann ◽  
Kefei Li ◽  
Myron Zaczkiewicz ◽  
Matthias Graf ◽  
Zhongmin Liu ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Experimental Work ◽  
Species Differences ◽  
Experimental Studies ◽  
Published Data ◽  
Causative Role ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Human Material

The role of C-reactive protein (CRP) in atherosclerosis is controversially discussed. Whereas initial experimental studies suggested a pathogenic role for CRP in atherogenesis, more recent genetic data from Mendelian randomization trials failed to provide evidence for a causative role of CRP in cardiovascular disease. Also, experimental results from laboratories all over the world were indeed contradictory, partly because of species differences in CRP biology and partly because data were not accurately evaluated. Here we summarize the published data from experimental work with mainly human material in order to avoid confusion based on species differences in CRP biology. Experimental work needs to be reevaluated after reconsideration of some traditional rules in research: (1) in order to understand a molecule’s role in disease it may be helpful to be aware of its role in physiology; (2) it is necessary to define the disease entity that experimental CRP research deals with; (3) the scientific consensus is as follows: do not try to prove your hypothesis. Specific CRP inhibition followed by use of CRP inhibitors in controlled clinical trials may be the only way to prove or disprove a causative role for CRP in cardiovascular disease.

Hypothyroidism and cardiovascular system

2016 ◽  
Vol 94 (7) ◽  
pp. 497-503 ◽  
Author(s):  
A. F. Verbovoy ◽  
Lyudmila A. Sharonova ◽  
O. V. Kosareva ◽  
N. I. Verbovaya ◽  
Yu. A. Dolgikh
Keyword(s):  
Risk Factors ◽  
Cardiovascular Disease ◽  
Cardiovascular Diseases ◽  
Vitamin D3 ◽  
Thyroid Dysfunction ◽  
Myocardial Remodeling ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
The Relationship

The article presents data on the relationship between thyroid dysfunction and cardiovascular diseases. The role of dyslipidemia, adipokines (adiponectin, leptin, resistin), C-reactive protein, deficiency of vitamin D3 in the development of cardiovascular disease in hypothyroidism is discussed. The article describes characteristics of myocardial remodeling, its dysfunction and their correlation with risk factors of cardiovascular diseases in patients with hypothyroidism.

scholarly journals The Interaction of C - Reactive Protein, Bisphenol A, & Cardiovascular Disease: A Demographical Analysis

2016 ◽  
Vol 9 (3) ◽  
pp. 63 ◽  
Author(s):  
Hassan Naji
Keyword(s):  
Cardiovascular Disease ◽  
Bisphenol A ◽  
Quantitative Research ◽  
The Body ◽  
Spearman Correlation ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
The Impact ◽  
The Relationship

<p><strong>OBJECTIVE: </strong>The main objective of the study was to investigate the role of C-reactive protein on the relationship between Bisphenol A &amp; Cardiovascular Disease, where the C-reactive protein has been taken as a moderating variable.</p><p><strong>METHODS: </strong>Quantitative research design has been incorporated for evaluating the role of C-reactive protein. Similarly, non-parametric Spearman correlation test has been conducted to assess the relationship between BPA and CVD. The data was taken out from the National Health and Nutrition Examination Survey (NHANES), which was collected in the year 2009-2010.</p><p><strong>RESULTS: </strong>The impact of urinary Bisphenol A on serum C-reactive protein was found statistically significant according to the Spearman correlation coefficient, <em>r</em>s<em>= </em>.06, <em>p </em>= .015. The scatter plots found that there is no relationship between the two variables; this observation held true after filtering the outliers from the plot.</p><p><strong>CONCLUSION:</strong> The results might have positive change by contributing to the body of knowledge on bisphenol A and by rising scientific examination of substances used by the people in the daily life. Further research to identify other possible causes of CVD and elevation of CRP is recommended.</p>

Role of Hypoalbuminemia in the Genesis of Cardiovascular Disease in Dialysis Patients

1999 ◽  
Vol 19 (2_suppl) ◽  
pp. 144-149 ◽  
Author(s):  
Soon Bae Kim ◽  
Won Seok Yang ◽  
Jung Sik Park
Keyword(s):  
Cardiovascular Disease ◽  
Cell Injury ◽  
Ldl Cholesterol ◽  
C Reactive Protein ◽  
Dialysis Patients ◽  
Reactive Protein ◽  
Acid Metabolites ◽  
Von Willebrand ◽  
Willebrand Factor

Our objective was to review the articles about the association between hypoalbuminemia and atherosclerotic or thrombotic cardiovascular disease (CVD) and to look for possible explanations for the role of hypoalbuminemia. Increased incidences of CVD were reported in patients with hypoalbuminemia owing to renal or other diseases. Hypoalbuminemia increases plasma levels of lipoprotein(a), fibrinogen, and arachidonic acid metabolites; it also increases platelet aggregability and blood viscosity, all of which may contribute to the development of CVD. This cause-effect association is thought to be “dependent.” Changes in atherogenic lipoproteins or lipids, such as LDL cholesterol, triglycerides, and apolipoprotein B, are controversial in hypoalbuminemic dialysis patients, possibly because coexistent malnutrition and volume status can affect both albumin and lipids. In our recent study, there was a negative correlation between serum albumin and C-reactive protein, D-dimer (an index of intravascular thrombogenesis), and von Willebrand factor (a marker for endothelial cell injury), but infusion of albumin did not affect the level of these parameters, which suggests that the correlations may be an effect-effect association by a confounding variable, such as inflammation. In conclusion, hypoalbuminemia is associated with cardiovascular disease via two pathways: one, a “dependent” cause-effect association; the other, an effect-effect association.

The Emerging Role of Inflammation in Cardiovascular Disease

2018 ◽  
Vol 52 (8) ◽  
pp. 801-809 ◽  
Author(s):  
Brandon K. Martinez ◽  
C. Michael White
Keyword(s):  
Cardiovascular Disease ◽  
English Language ◽  
Data Extraction ◽  
High Sensitivity ◽  
Atherosclerotic Cardiovascular Disease ◽  
C Reactive Protein ◽  
Converting Enzyme Inhibitors ◽  
Reactive Protein ◽  
The Impact

Objective: To review the role of inflammatory suppression in patients with atherosclerotic cardiovascular disease (ASCVD) with a focus on the interleukin-1β blocker canakinumab. Data Sources: An Ovid MEDLINE literature search (1946 to February 2018) was performed using search terms inflammation, ASCVD, atherosclerosis, C-reactive protein, canakinumab. Additional references were identified from a review of literature citations. Study Selection and Data Extraction: English-language studies assessing the impact of pharmacological agents, including canakinumab, on inflammation as measured by high-sensitivity C-reactive protein (hsCRP) and the association with reducing ASCVD events were evaluated. Data Synthesis: Nine studies were included to describe the effect of ASCVD drugs on hsCRP. Aspirin, angiotensin-converting enzyme inhibitors, gemfibrozil, and statins exhibit varying degrees of hsCRP reduction and are associated with a reduction of ASCVD events. The Canakinumab Antiinflammatory Thrombosis Outcome Study (CANTOS), showed a significant reduction of ASVCD events in patients with elevated baseline hsCRP levels without affecting cholesterol. Conclusions: Patients with elevated inflammatory markers such as hsCRP are at risk for ASVCD events. Several drug classes have shown the ability to decrease hsCRP levels, but the extent to which this reduces ASCVD events in lieu of other drug mechanisms was not clear. Canakinumab specifically targets the inflammatory process in ASCVD and was proven to be effective in preventing ASCVD events in patients with elevated hsCRP levels.

The Role of C-Reactive Protein in Atherosclerotic Cardiovascular Disease: An Overview

2008 ◽  
Vol 6 (4) ◽  
pp. 258-270 ◽  
Author(s):  
Eleni Nakou ◽  
Evangelos Liberopoulos ◽  
Haralampos Milionis ◽  
Moses Elisaf
Keyword(s):  
Cardiovascular Disease ◽  
Atherosclerotic Cardiovascular Disease ◽  
C Reactive Protein ◽  
Reactive Protein

scholarly journals Inhibiting C-Reactive Protein for the Treatment of Cardiovascular Disease: Promising Evidence from Rodent Models

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Alexander J. Szalai ◽  
Mark A. McCrory ◽  
Dongqi Xing ◽  
Fadi G. Hage ◽  
Andrew Miller ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Heart Function ◽  
Controlled Trial ◽  
Disease Process ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Cardiovascular Damage ◽  
A Prospective Study ◽  
Control Study

Raised blood C-reactive protein (CRP) level is a predictor of cardiovascular events, but whether blood CRP is causal in the disease process is unknown. The latter would best be defined by pharmacological inhibition of the protein in the context of a randomized case-control study. However, no CRP specific drug is currently available so such a prospective study cannot be performed. Blood CRP is synthesized primarily in the liver and the liver is an organ where antisense oligonucleotide (ASO) drugs accumulate. Taking advantage of this we evaluated the efficacy of CRP specific ASOs in rodents with experimentally induced cardiovascular damage. Treating rats for 4 weeks with a rat CRP-specific ASO achieved >60% reduction of blood CRP. Notably, this effect was associated with improved heart function and pathology following myocardial infarction (induced by ligation of the left anterior descending artery). Likewise in human CRP transgenic mice treated for 2 weeks with a human CRP-specific ASO, blood human CRP was reduced by >70% and carotid artery patency was improved (2 weeks after surgical ligation). CRP specific ASOs might pave the way towards a placebo-controlled trial that could clarify the role of CRP in cardiovascular disease.

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