SynthesisBMC medical genetics2014
Association of cholesteryl ester transfer protein (CETP) gene polymorphism, high density lipoprotein cholesterol and risk of coronary artery disease: a meta-analysis using a Mendelian randomization approach.
Synthesis in BMC medical genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Causal association between lipoproteins and risk of coronary artery disease-a systematic review and meta-analysis of Mendelian randomization studies.Clinical research in cardiology : official journal of the German Cardiac Society · 2026Pooled it
- Effects of exercise training on carotid intima-media thickness in patients with type 2 diabetes and coronary artery disease. Influence of carotid plaques.Cardiovascular diabetology · 2016Trial
- Lipids at the Nexus between Cerebrovascular Disease and Vascular Dementia: The Impact of HDL-Cholesterol and Ceramides.International journal of molecular sciences · 2023Review
- Saturated Fat and Cardiovascular Health: Phenotype and Dietary Factors Influencing Interindividual Responsiveness.Current atherosclerosis reports · 2022Review
- Hyperalphalipoproteinemia and Beyond: The Role of HDL in Cardiovascular Diseases.Life (Basel, Switzerland) · 2021Review
- The causal role of elevated uric acid and waist circumference on the risk of metabolic syndrome components.International journal of obesity (2005) · 2020Article
- Article
- HDL Cholesterol as a Marker of Disease Severity and Prognosis in Patients with Pulmonary Arterial Hypertension.International journal of molecular sciences · 2019Review
- The Role of High-Density Lipoproteins in Diabetes and Its Vascular Complications.International journal of molecular sciences · 2018Review
- Biomarkers and Gene Polymorphisms in Members of Long- and Short-lived Families: A Longevity Study.The open cardiovascular medicine journal · 2018Article
- HDL and atherosclerotic cardiovascular disease: genetic insights into complex biology.Nature reviews. Cardiology · 2018Review
- HDL Cholesterol Metabolism and the Risk of CHD: New Insights from Human Genetics.Current cardiology reports · 2017Review
- The association of APOC4 polymorphisms with premature coronary artery disease in a Chinese Han population.Lipids in health and disease · 2015Article
- A common genetic variation in CEBPE and acute lymphoblastic leukemia: a meta-analysis of the available evidence.OncoTargets and therapy · 2015Article
- Cholesteryl ester transfer protein: ace of spades, queen of hearts, or the joker?Frontiers in pharmacology · 2015Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRecent randomized controlled trials have challenged the concept that increased high density lipoprotein cholesterol (HDL-C) levels are associated with coronary artery disease (CAD) risk reduction. The causal role of HDL-C in the development of atherosclerosis remains unclear. To increase precision and to minimize residual confounding, we exploited the cholesteryl ester transfer protein (CETP)-TaqIB polymorphism as an instrument based on Mendelian randomization.
methodsThe Mendelian randomization analysis was performed by two steps. First, we conducted a meta-analysis of 47 studies, including 23,928 cases and 27,068 controls, to quantify the relationship between the TaqIB polymorphism and the CAD risk. Next, the association between the TaqIB polymorphism and HDL-C was assessed among 5,929 Caucasians. We further employed Mendelian randomization to evaluate the causal effect of HDL-C on CAD based on the findings from the meta-analysis.
resultsThe overall comparison of the B2 allele with the B1 allele yielded a significant risk reduction of CAD (P < 0.0001; OR = 0.88; 95% CI: 0.84-0.92) with substantial between-study heterogeneity (I² = 55.2%; P(heterogeneity) <0.0001). The result was not materially changed after excluding the Hardy-Weinberg Equilibrium (HWE)-violation studies. Compared with B1B1 homozygotes, Caucasian carriers of the B2 allele had a 0.25 mmol/L increase in HDL-C level (95% CI: 0.20-0.31; P <0.0001; I² = 0; P(heterogeneity) =0.87). However, a 1 standard deviation (SD) elevation in HDL-C levels due to the TaqIB polymorphism, was marginal associated with CAD risk (OR =0.79; 95% CI: 0.54-1.03; P =0.08).
conclusionsTaken together, our results lend support to the concept that increased HDL-C cannot be translated into a reduction in CAD risk.
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