Fig. 7: Integration of human GWAS data reveals vascular disease risk genes that are induced by obesity.

a, Comparison of known high-risk variants (identified via GWAS) for coronary artery disease with obesity-induced gene expression changes in heart art ECs at the 6-month timepoint. b, Comparison of known high-risk variants for atherosclerosis with obesity-induced gene expression changes in heart art ECs at the 6-month timepoint. c, Comparison of known high-risk variants for heart failure with obesity-induced gene expression changes in heart art ECs at the 6-month timepoint. d, Expression levels of Sox17, the most significant genetic risk factor for pulmonary arterial hypertension (PAH), in pulmonary art ECs in obesity and after reversion. e–i, Comparison of known high-risk variants for hypertension with obesity-induced gene expression changes in lung art (e), heart art (f), kidney art (g), kidney gEC (h) and brain art (i) ECs at the 6-month timepoint. j, Comparison of known high-risk variants for stroke with obesity-induced gene expression changes in brain art ECs at the 6-month timepoint. k, Comparison of known high-risk variants for Alzheimer’s disease with obesity-induced gene expression changes in brain cap ECs at the 6-month timepoint. l, Comparison of known high-risk variants for bipolar disorder with obesity-induced gene expression changes in brain cap ECs at the 6-month timepoint. m–r, Summary of the most prominent obesity-induced gene expression changes in EC populations identified in this study. Changes in EC populations of the AT (m), liver (n), heart (o), lungs (p), kidneys (q) and brain (r) are provided. Genes indicated in red are high-risk genes for the development of vascular pathologies and overlap with human GWAS studies. The x axes in a–c and e–l represent the –log10 (P value) of disease-associated SNPs assigned to a gene, while the y axes in a–l represent the log (FC) of the marked gene in obesity. Genes with | log (FC) | > 0.1 are highlighted in red. Select candidate genes are labeled. SNPs associated with each disease were obtained from the NHGRI-EBI GWAS database.