Skip to main content
. Author manuscript; available in PMC: 2020 Apr 1.
Published in final edited form as: Trends Pharmacol Sci. 2019 Feb 28;40(4):253–266. doi: 10.1016/j.tips.2019.02.004

Table 1.

Role of MSTFs in atherosclerosis in vivo

Animal model Effect on
atherosclerosis
Observed atherosclerotic characteristics References
KLF2+/−; ApoE−/− mice Foam cell formation [36]
KLF2 ΔMye; LDLR−/− mice Lesional neutrophils and macrophages [38]
KLF4 ΔEC; ApoE−/− Endothelial inflammation and thrombosis [35]
KLF4Tg(EC); ApoE−/− Endothelial inflammation and thrombosis [35]
NRF2−/−; ApoE−/− Foam cell formation [95, 96]
NRF2−/−; LDLR−/− ApoB 100/100 Mixed Atherosclerotic lesion size
Atherosclerotic plaque vulnerability
[97]
NF-kBΔEC; ApoE−/− Adhesion molecules and inflammation [63]
I-κBmtOE(EC); ApoE−/− Chronic intermittent hypoxia induced atherosclerosis; NF-kB activity [64]
HIF-1αΔEC; ApoE−/− Monocyte adhesion [61]
HIF-1αΔMye; ApoE−/− Inflammatory gene expression [98]
YAP/TAZKD; ApoE−/− Promotes EC proliferation, inflammation [27]
YAPOE (EO); ApoE−/−; YAPTg (EC); ApoE−/−; YAP/TAZCA; ApoE−/− Monocyte adhesion, macrophage accumulation [26]
YApOE (EC); ApoE−/− VCAM1 dependent monocyte adhesion [28]

Abbreviations:

KD, knockdown; OE (EC), endothelial cell-specific overexpression; Tg (EC), endothelial cell specific transgene; ΔMye, myeloid cell-specific knockout; ΔEC, endothelial cell-specific knockout