Lindsey K. Stolze

This study identifies inflammation-induced alternative splicing in human endothelial cells and links it to cardiovascular disease risk through genetic mechanisms.

The paper integrates proteomics and transcriptomics with genetic analyses to identify molecular mechanisms and targets of coronary artery disease.

This study examines cytokine and chemokine receptor expression in adipose tissue endothelial cells of HIV-positive individuals, identifying receptor differences and their potential role in vascular dysfunction.

The paper identifies a CAD risk SNP rs880890 in an endothelial enhancer that reduces CALCRL expression by impairing HSF binding under shear stress.

This study profiles human aortic endothelial cells in vitro and atherosclerotic lesions ex vivo, revealing heterogeneous subtypes and their responses to perturbations.

The paper identifies functional non-coding SNPs in human endothelial cells that influence vascular traits by affecting transcriptional regulation and chromatin states.

The paper systematically analyzes naturally occurring insertions and deletions (InDels) to assess their impact on transcription factor spacing and identifies tolerant and sensitive TF pairs.

This study identifies a genetic variant at 1p32.2 that regulates endothelial responses to hemodynamics by modulating an enhancer region in vascular endothelium.