Why the study?
Does endothelial nitric oxide synthase (eNOS) overexpression inhibit atherosclerotic lesion formation in apoE-deficient mice on a high-cholesterol diet?
Population
Atherogenic apoE-deficient (apoE-KO) mice on a high-cholesterol diet
Comparison
Endothelial nitric oxide synthase overexpression… vs apoE-KO mice without eNOS overexpression
Design
Preclinical
Follow-up
8 to 12 weeks
Authors
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eNOS overexpression may accelerate atherosclerosis in hypercholesterolemic models; challenges consensus on NO protection and leaves open human relevance.
Does endothelial nitric oxide synthase (eNOS) overexpression inhibit atherosclerotic lesion formation in apoE-deficient mice on a high-cholesterol diet?
Chronic overexpression of eNOS accelerates rather than inhibits atherosclerosis in hypercholesterolemic mice due to eNOS dysfunction, an effect that can be mitigated by tetrahydrobiopterin supplementation.
Ozaki et al. (2002) studied this question.
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