Estimating the causal role of C-reactive protein in coronary heart disease: Collaborative mendelian randomization analysis

2010 ◽  
Vol 213 (1) ◽  
pp. e12
Author(s):  
F. Wensley
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Mendelian Randomization ◽  
Causal Role ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Mendelian Randomization Analysis ◽  
Randomization Analysis

scholarly journals CD28 Genetic Variants Increase Susceptibility to Diabetic Kidney Disease in Chinese Patients with Type 2 Diabetes: A Cross-Sectional Case Control Study

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Yangyang Li ◽  
Li Jin ◽  
Jing Yan ◽  
Hong Zhang ◽  
Rong Zhang ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Diabetic Kidney Disease ◽  
Mendelian Randomization ◽  
Costimulatory Molecule ◽  
Causal Role ◽  
Chinese Patients ◽  
Diabetic Kidney ◽  
Mendelian Randomization Analysis ◽  
Randomization Analysis

Few studies have illuminated the genetic role of T cell costimulatory molecule CD28/CD80/CTLA4 variants in diabetic kidney disease (DKD) susceptibility. We aimed to investigate the causal role of genetic polymorphisms in CD28/CD80/CTLA4 with DKD susceptibility in patients with T2DM. A total of 3253 patients with T2DM were recruited for genotyping: including 204 DKD patients and 371 controls in stage 1 and 819 DKD patients and 563 controls in stage 2; besides, 1296 T2DM patients were selected for the analysis of association between loci and DKD-related traits. A subset of 227 T2DM patients (118 patients with DKD and 109 patients without DKD) from the total population above were selected to assess serum soluble CD28 (sCD28) levels. Then, we performed a candidate gene association study to identify single-nucleotide polymorphisms (SNPs) associated with DKD susceptibility and further used those SNPs to perform Mendelian randomization analyses of serum sCD28 level and DKD susceptibility. Under additive genetic models, CD28-rs3116494 ( OR = 1.29 [95% CI 1.11, 1.51], P = 0.0011 ) and CD80-rs3850890 ( OR = 1.16 [95% CI 1.02, 1.31], P = 0.0283 ) were associated with DKD susceptibility adjusted for age, gender, body mass index (BMI), duration of diabetes, and HbA1c. CD28-rs3116494 was associated with serum sCD28 level ( β = 0.26 [95% CI 0.08, 0.44], P = 0.0043 ). The Mendelian randomization analysis showed that CD28-rs3116494 played a causal role in DKD by influencing serum sCD28 levels ( β = 1.15 [95% CI 0.46, 1.83], P = 0.0010 ). In conclusion, we identified that two novel SNPs, CD28-rs3116494 and CD80-rs3850890, were associated with DKD susceptibility. Using the Mendelian randomization analysis, our study provided evidence for a causal relationship between serum CD28 levels and DKD with T2DM in the Chinese population.

scholarly journals C-Reactive Protein and Coronary Heart Disease: All Said—Is Not It?

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Frederik Strang ◽  
Heribert Schunkert
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Experimental Studies ◽  
Epidemiological Studies ◽  
Experimental Investigations ◽  
C Reactive Protein ◽  
Genetic Studies ◽  
Reactive Protein ◽  
The Relationship

C-reactive protein (CRP) and coronary heart disease (CHD) have been the subject of intensive investigations over the last decades. Epidemiological studies have shown an association between moderately elevated CRP levels and incident CHD whereas genetic studies have shown that polymorphisms associated with elevated CRP levels do not increase the risk of ischemic vascular disease, suggesting that CRP might be a bystander rather than a causal factor in the progress of atherosclerosis. Beside all those epidemiological and genetic studies, the experimental investigations also try to reveal the role of CRP in the progress of atherosclerosis. 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.

scholarly journals Mendelian randomization analysis supports the causal role of dysglycaemia and diabetes in the risk of coronary artery disease

2015 ◽  
Vol 36 (23) ◽  
pp. 1454-1462 ◽  
Author(s):  
Stephanie Ross ◽  
Hertzel C. Gerstein ◽  
John Eikelboom ◽  
Sonia S. Anand ◽  
Salim Yusuf ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Mendelian Randomization ◽  
Causal Role ◽  
Mendelian Randomization Analysis ◽  
Artery Disease ◽  
Randomization Analysis

scholarly journals Sex Differences in the Risk of Coronary Heart Disease Associated With Type 2 Diabetes: A Mendelian Randomization Analysis

Diabetes Care ◽  
2020 ◽  
pp. dc201137
Author(s):  
Tricia M. Peters ◽  
Michael V. Holmes ◽  
J. Brent Richards ◽  
Tom Palmer ◽  
Vincenzo Forgetta ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Coronary Heart Disease ◽  
Sex Differences ◽  
Heart Disease ◽  
Mendelian Randomization ◽  
Mendelian Randomization Analysis ◽  
Randomization Analysis

scholarly journals Association of high sensitive C-reactive protein with coronary heart disease: a Mendelian randomization study

2019 ◽  
Vol 20 (1) ◽  
Author(s):  
Qian Zhuang ◽  
Chong Shen ◽  
Yanchun Chen ◽  
Xianghai Zhao ◽  
Pengfei Wei ◽  
...  
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Regression Model ◽  
Mendelian Randomization ◽  
Cox Regression ◽  
Causal Effect ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Hs Crp

Abstract Objectives Whether high sensitivity C-reactive protein (hs-CRP) has a causal effect on coronary heart disease (CHD) is unclear. This study investigated the causal effect of hs-CRP on CHD risk using Mendelian Randomization (MR) analysis. Methods A total of 3802 subjects were recruited in the follow-up study. Linear regression model was used to evaluate the relationship between CRP polymorphisms and hs-CRP. Survival receiver operator characteristic curve method was used to explore the cut-off of hs-CRP on CHD incidence. Cox regression model was applied to detect the association of hs-CRP with CHD by calculating the hazard ratio (HR) and 95% confidence interval (CI). Rs1205 and rs876537 in CRP were selected as instrumental variables in MR analysis. Results During a median follow-up time of 5.01 years, 98 CHD incidence was identified (47.03/104 person-years). Hs-CRP was significantly increased among rs1205 and rs876537 genotypes with r values of 0.064 and 0.066, respectively. Hs-CRP 1.08 mg/L was identified as the cut-off value with a maximum value of sensitivity and specificity on prediction of CHD. Participants with ≥1.08 mg/L of hs-CRP has a higher risk of CHD incidence than that of participants with < 1.08 mg/L, the adjusted HR (95% CI) was 1.69 (1.11–2.60) with a P value of 0.016. No significant casual association was observed between hs-CRP and CHD with a P value of 0.777. Conclusions The association between hs-CRP and CHD is unlikely to be causal, hs-CRP might be a predictor for incidence of CHD in general population.

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