Accelerated Atherosclerosis, Aortic Aneurysm Formation, and Ischemic Heart Disease in Apolipoprotein E/Endothelial Nitric Oxide Synthase Double-Knockout Mice

By P. Kuhlencordt, R. Gyurko, F. Han, M. Scherrer-Crosbie, T. Aretz, R. Hajjar, M. Picard, Paul L Huang. Circulation, 2001

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Endothelial Cell Dysfunction and the Pathobiology of Atherosclerosis (2016, positive): “Furthermore, these eNOS-deficient mice were found to display increased endothelial–leukocyte interactions, platelet aggregation, and thrombosis,(80,81) and, when crossed with ApoE-deficient (hypercholersterolemic) mice, developed accelerated atherosclerosis.(82) In a classic study, the clinical sign”
Reactive Oxygen Species in Cardiovascular Disease (2011, background): “Data on atherosclerosis support this contention as eNOS-null animals on an apolipoprotein E (ApoE)-null background exhibit more atherosclerosis than ApoE-null mice alone [113], whereas overexpression of eNOS in ApoE-null mice shown increased atherosclerotic lesion formation with elevated levels of v”
The pathobiology of diabetic complications: a unifying mechanism. (2005, background): “However, when the apoE knockout mouse is crossed with an eNOS knockout mouse, the early atherosclerotic lesions are nearly doubled simply by loss of eNOS activity (51).”