Table 5. Altered cardiovascular disease pathways in adult F1 mice treated with caffeine during E6.5–9.5.
Pathways | p-value | Activation z-scorea | Genes |
---|---|---|---|
Infarction | 3.47E-06 | −2.750 | ACTA1,APOE,C1QA,CD55,FSTL1,GDF15,GPX1,HLA-A,PTGDS,STAT1,TNFRSF12A |
Myocardial infarction | 8.08E-04 | −1.992 | ACTA1,APOE,CD55,FSTL1,GDF15,STAT1 |
Permeability of vascular system | 8.44E-03 | −1.969 | APOE,AQP4,FGFBP3,TNFRSF12A |
Size of infarct | 3.31E-06 | −1.673 | APOE,C1QA,GDF15,GPX1,HLA-A,PTGDS,STAT1,TNFRSF12A |
Vasculogenesis | 6.05E-03 | −1.109 | ABRA,APOE,C1QA,GPX1,HLA-DQB1,KLK3,SEMA3B,STAT1,THBS4,TNFRSF12A,WARS |
Adhesion of endothelial cells | 6.33E-03 | −0.293 | C1QA,CD274,GDF15,STAT1 |
Lesioning of aorta | 9.10E-07 | APOE,GPX1,NPC1 | |
Peripheral vascular disease | 8.48E-03 | APOE,AQP4,CFH,GPX1,MARK1,SEMA3B,TNFRSF12A | |
Size of vascular lesion | 7.61E-03 | APOE,C1QA,GPX1 | |
Advanced stage peripheral arterial disease | 6.89E-03 | APOE,CFH,MARK1,SEMA3B | |
Thickness of heart ventricle | 6.70E-03 | APOE,KLK3 | |
Cellularity of atherosclerotic lesion | 2.05E-05 | APOE,NPC1 | |
Function of cardiovascular system | 1.18E-03 | ABRA,APOE,AQP4,CD55,CFP,GDF15,GPX1,KLK3 | |
Thrombosis | 1.16E-02 | APOE,C1QA,CFH,GDF15 | |
Mass of left ventricle | 1.05E-02 | KLK3,THBS4 |
aA positive z-score means the pathway is activated, and a negative z-score indicates the pathway is inhibited.