Chen‐Yang Su

The paper constructs a genomic atlas of cardiac and adiposity imaging phenotypes using whole-genome sequencing data from UK Biobank, identifying genetic associations and polygenic scores linked to cardiometabolic diseases.

This study identifies ancestry-specific APOE effects on phenotypes and plasma proteins in diverse populations, highlighting the need for ancestry-aware risk interpretation.

This paper identifies nine circulating proteins associated with heart failure beyond the genetic component shared with BMI using GWAS-by-subtraction and proteome-wide Mendelian randomization.

This paper identifies 29 circulating proteins associated with type 2 diabetes risk independent of BMI using GWAS-by-subtraction, proteome-wide Mendelian randomization, and colocalization analyses.

This study identifies 36 circulating proteins associated with a shared genetic liability for schizophrenia, depression, and bipolar disorder using genomic and proteomic data.

The paper uses Mendelian randomization to show that current disease-mortality GWAS may lack sufficient power to detect shared genetic effects, despite strong associations in case-control studies.

The paper maps adipokine-associated variants to effector genes across 1,669 traits, identifying TGFB2 and VEGFA as linked to insulin resistance and distinct disease risks.

This study uses proteome-wide Mendelian randomization to identify 18 circulating proteins causally linked to bone mineral density and fracture risk, with TIMP2 showing strong associations with lower BMD and increased fracture risk.

This study uses Mendelian randomization to identify circulating proteins associated with cardiovascular traits in African-ancestry populations and finds four proteins uniquely linked to lipids and heart diseases in this group.

This paper identifies risk proteins for intracranial aneurysms using multi-ancestry proteogenomic analysis and finds ADH4 and PLEKHA1 as non-blood pressure-mediated candidates.

This study identifies OA-specific genetic effects and novel therapeutic targets by separating OA genetics from those shared with obesity using GWAS and proteomics data.

MR Corge performs sensitivity analysis for Mendelian randomization by identifying core instruments to reduce horizontal pleiotropy bias and improve causal effect estimation.

This study uses proteome-phenome-wide Mendelian randomization across three ancestries to identify protein-phenotype associations and potential therapeutic targets.

The paper identifies nephronectin as a mediator of obesity's effect on COVID-19 severity using proteome-wide Mendelian randomization and validates its expression in lung cells.

This study uses whole-exome sequencing to directly call HLA alleles in the UK Biobank, identifying 129 novel associations between HLA alleles and 11 autoimmune diseases.