Marcus Edi Kleber

This study identifies COPI coatomer subunits that regulate LDL receptor activity, apoB secretion, and hepatic lipid storage, with genetic variants linked to elevated LDL-C levels.

This study uses whole genome sequencing to identify 18 novel genetic loci associated with plasma fibrinogen levels, including variants more common in African populations and linked to liver-related traits and disease.

This study shows that a genetic risk score for coronary artery calcification improves CAD prediction beyond traditional risk factors in three European cohorts.

The paper identifies PSKH2 as a gene influencing variability in Factor V plasma activity through genome-wide analysis of non-additive allele effects.

This study uses GWAS and Mendelian randomization to show that lower sclerostin levels increase risk of hypertension, type 2 diabetes, myocardial infarction, and atherogenic lipid profiles.

The paper examines nc886 methylation across populations and tissues, finding stable levels except in specific tissues and some discordance in dizygotic twins.

This study identifies 242 genetic loci for glycaemic traits using trans-ancestry meta-analysis, finding 99 novel loci and improved fine-mapping resolution compared to single-ancestry analyses.

This study conducts a large GWAS on heart failure, identifying 12 genetic loci with associations to CAD, atrial fibrillation, and reduced left ventricular function, and provides causal evidence for several risk factors.

This paper uses Mendelian Randomization to show that higher circulating sclerostin levels causally reduce bone mineral density and increase fracture risk.

This paper evaluates the causal effect of fibrinogen on coronary heart disease using Mendelian randomization, finding a small effect with multi-variant methods but not with single variant approaches.

The paper identifies cis-epistasis at the LPA locus involving two SNPs that interact to modulate coronary artery disease risk and related traits.

The paper assesses if genetic risk for atrial fibrillation explains cardioembolic stroke risk using genome-wide data from the Stroke Genetics Network.