Key result
Deficiency of NPR2 in mice impaired aortic valve function, increased valve thickening, and resulted in a 9.4% incidence of congenital bicuspid aortic valves.
Why the study?
Does deficient CNP/NPR2 signaling cause accelerated progression of aortic valve disease in mice?
Population
Cultured porcine valve interstitial cells, Npr2 +/- and Npr2 +/- ; Ldlr -/- mice, and wild-type littermate…
Comparison
Deficient CNP/NPR2 signaling (Npr2 +/- genotype) vs Wild-type littermate controls
Design
Preclinical
Authors
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NPR2 deficiency links to aortic valve disease in mice; hypothesis-generating for CNP/NPR2-targeted therapies in humans.
Does deficient CNP/NPR2 signaling cause accelerated progression of aortic valve disease in mice?
Deficiency in CNP/NPR2 signaling promotes bicuspid aortic valves, aortic valve disease, left ventricular dysfunction, and ascending aortic dilatations in mice, highlighting a potential therapeutic target.
Blaser et al. (2017) studied Aortic valve disease. Npr2 +/- mutation (deficient CNP/NPR2 signaling) vs. Wild-type littermate controls was evaluated on Incidence of congenital bicuspid aortic valves. Deficiency of NPR2 in mice impaired aortic valve function, increased valve thickening, and resulted in a 9.4% incidence of congenital bicuspid aortic valves.
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