Population
eNOS mice and wild-type mice; in vitro cultures of valve interstitial cells and aortic valve endothelial cells
Comparison
eNOS deficiency and coculture with vlvECs vs Wild-type mice and VICs cultured alone
Design
Preclinical
Follow-up
6 and 18 months (in vivo)
Authors
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No immediate clinical implications for aortic valve disease; hypothesis-generating for eNOS protection against bicuspid valve calcification.
Endothelial nitric oxide synthase deficiency promotes fibrosis in all aortic valves but calcification specifically in bicuspid aortic valves, highlighting a protective role of endothelium-derived nitric oxide.
Accaoui et al. (2014) studied this question.
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