Tom R. Webb

This study identifies distinct gene expression changes in human coronary artery endothelial cells under elevated flow compared to oscillatory and normal flow, highlighting unique regulatory effects on CAD-related pathways and alternative splicing.

This study identifies genetic determinants of endothelial cell molecular traits and their overlap with disease GWAS loci, revealing shared and unique mechanisms in non-communicable diseases.

The paper identifies and validates novel regulators of vascular smooth muscle cell proliferation using network analysis and experimental validation, highlighting RUNX1 and the TIMP1-CD74 axis as potential therapeutic targets.

The paper identifies and characterizes 329 novel long non-coding RNAs in vascular smooth muscle cells, finding they are mostly antisense transcripts with cytoplasmic localization and miRNA targets.

This study identifies 17 genetic risk loci for spontaneous coronary artery dissection (SCAD), including 12 new ones, and highlights genes related to artery integrity and coagulation.

A coronary artery disease GWAS of 181,522 cases among 1,165,690 participants yields 241 associations (54 new); an eight-predictor consensus nominates 185 candidate causal genes, 94 with ≥3 predictors.

The paper identifies rare loss-of-function mutations in PTGIR in FMD and SCAD patients, showing impaired prostacyclin receptor function and suggesting a role for prostacyclin signaling in these diseases.

This paper develops a genomic risk score for coronary artery disease using 1.7 million variants and tests it in UK Biobank, showing it outperforms conventional risk factors in predicting CAD risk.