Aldons Jake Lusis

The paper identifies a TMAO locus on mouse chromosome 12 modified by sex and diet through a meta-analysis of 1,482 Diversity Outbred mice.

The paper uses sex-stratified analyses to explore genetic architecture of complex traits in mice and humans, finding high concordance in allelic effect directions and suggesting new methods for identifying biologically significant associations.

This study shows TMAO affects cell type-specific pathways in mouse aorta, promoting atherosclerotic plaque instability by increasing apoptosis and reducing ECM formation.

This study shows that PPARγ controls adipose tissue expansion by regulating LPCAT3, which affects membrane lipid composition and triglyceride storage, linking dietary n-6 PUFAs to energy balance.

This study shows that reducing Glo1 in mice causes age- and sex-dependent metabolic issues like obesity and altered lipid metabolism without significant changes in AGEs.

This study identifies genetic loci linking host amylase genes to gut microbiome composition and metabolic traits in hyperlipidemic mice.

This study investigates the causal relationship between circulating glycine levels and atherosclerosis using genetic analyses in humans and dietary experiments in mice, finding no strong causal evidence despite observational associations.

This study identifies shared and distinct genetic pathways between human and mouse in coronary artery disease using multi-omics data and GWAS, showing over 75% shared pathways.

This study investigates the genetic basis of dietary iron overload and associated pathologies in mice using the Hybrid Mouse Diversity Panel, identifying genetic loci and pathways involved.

The paper identifies three genetic loci influencing mitochondrial proteins and heart hypertrophy in mice using proteomics and association mapping.

This study shows that fructose metabolism via KHK-C increases ER stress and modulates the hepatic transcriptome, contributing to NAFLD progression in both genetic and diet-induced models.

The paper identifies UFMylation as a negative regulator of skeletal muscle function through proteome-wide systems genetics in mice and validates it in a disease model.

This study uses transcriptome-wide association analysis to identify 114 genes associated with coronary artery disease, including 18 novel genes, and shows they are enriched in lipid metabolism pathways.

This study identifies genetic links between gut microbiota, lipids, and host transcripts in mice, revealing key roles for Akkermansia muciniphila and ornithine lipids in microbe-host interactions.

The paper identifies placental gene-trait associations across the life course using multi-omics data, finding genetic effects on early-life traits but not later ones.

The paper identifies 31 host genetic loci influencing gut microbiome composition through GWAS and suggests causal effects in inflammatory diseases.

The paper develops a statistical test to detect polygenic epistasis by analyzing genotype-by-ancestry interactions in mice and yeast, finding significant associations across multiple phenotypes.

This study shows that gut microbiota differences between mouse strains contribute to varied metabolic responses to high fructose consumption, with Akkermansia playing a key protective role.

The paper identifies genetic regulation of HDL proteome variation across mouse strains, revealing coordinated protein regulation and functional diversity in HDL subspecies.

The paper identifies DNA methylation associations with metabolic syndrome traits in adipose tissue and develops a biomarker for type II diabetes risk.

The paper identifies disease-associated genes missed by traditional methods using a personalized differential gene expression analysis in a genetically diverse mouse model of cardiac hypertrophy and heart failure.

The paper identifies PPP1R3A as a central cardioprotective factor in pressure overload heart failure by analyzing gene network rewiring in human hearts.