Peter W.F. Wilson

The paper identifies 800 exome-wide significant rare coding variants associated with blood lipids in over a million diverse individuals, including 130 driven by non-European-like populations.

This study conducts an X-chromosome-wide association study to identify genetic signals for heart failure and its subtypes, finding novel loci and replicating some in UK Biobank.

This study conducts a multi-ancestry GWAS of rheumatoid arthritis using the VA Million Veteran Program, identifying 152 genome-wide significant loci and improving fine-mapping resolution.

This study identifies two independent BMI-associated variants at the GLP1R locus with distinct associations with T2D risk, suggesting heterogeneous genetic mechanisms.

This study identifies novel genetic signals associated with severe obesity through GWAS and shows strong genetic overlap with BMI, highlighting shared comorbidities and lifestyle interactions.

This paper develops a semi-empirical Bayesian framework to calibrate weak instrumental bias in sex-specific Mendelian randomization studies, revealing significant sex differences in causal effects of sleep phenotypes on cardiovascular diseases.

This paper conducts a multi-ancestry GWAS of sleep duration, identifying 234 genome-wide significant loci and showing distinct genetic architecture from other sleep and psychiatric traits.

The paper performs GWAS on cardiovascular outcomes in CKD patients, identifying stroke-associated SNVs but not replicating CHD findings, and finding genetic correlations with published GWAS.

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 uses Mendelian randomization to identify two proteins, CCL27 and TNFRSF14, that influence subsequent cardiovascular events after a stroke, suggesting inflammation as a contributing factor.

This study identifies six novel genetic loci associated with BMI change over adulthood using UK Biobank health records, finding lower heritability for BMI change compared to baseline BMI.

This paper corrects collider bias in a GWAS of diabetes-related heart failure, identifying novel loci and showing bidirectional genetic associations between T2D and HF.

This study identifies novel genetic risk variants and potential drug targets for heart failure using GWAS and Mendelian randomization proteomics.

This study conducts a GWAS of obstructive sleep apnea in the Million Veteran Program, identifying sex-specific genetic loci and highlighting genetic heterogeneity by sex.

This study compares the genetic architecture of heart failure with preserved ejection fraction (HFpEF) and reduced ejection fraction (HFrEF), finding distinct genetic associations and highlighting HFpEF's heterogeneity.

This study analyzes clonal hematopoiesis in over a million diverse individuals, identifying 72 genome-wide significant loci and linking CHIP to various phenotypes.

This study conducts a trans-ancestry GWAS using chronic ALT elevation as a proxy for NAFLD, identifies 77 significant loci, and validates 17 SNPs with histology and imaging data, revealing genetic links to metabolic and inflammatory traits.

This paper identifies two novel genetic loci associated with ischemic stroke and finds sex and ancestry differences in their effects.

This study shows that FH genetic variants increase CAD risk even after adjusting for multiple LDL-C measurements from EHRs, indicating LDL-C data alone cannot fully explain the risk.

This study performs multi-trait GWAS on atherosclerosis-related traits to identify novel pleiotropic loci and their potential biological mechanisms.

This study identifies 5,552 blood-cell trait-variant associations across 746,667 individuals from 5 global populations, including 71 novel loci and ancestry-specific variants not found in European ancestry populations.

This study identifies 5,106 new genetic variants associated with blood cell traits using large-scale GWAS, highlighting the polygenic and monogenic basis of hematopoiesis.

This study shows smoking increases type 2 diabetes risk through BMI, but not coronary artery disease risk, using Mendelian randomization.

Multi-ethnic type 2 diabetes (T2D) meta-analysis of 228,499 cases and 1,178,783 controls finds 318 previously unreported loci, 804 expression-colocalized genes, and 13 SNP-by-T2D vascular-outcome interactions.

This study identifies 14 genome-wide significant loci and a polygenic signature for myeloproliferative neoplasms, implicating hematopoietic stem cell function and self-renewal in disease risk.