Why the study?
Congenital heart defects frequently involve semilunar valve malformations, but the role of Gata4 in semilunar valve development and stenosis remained to be characterized.
Population
Gata4G295Ski/wt mouse model
Design
Preclinical animal model study
Follow-up
Up to 1 year of age
Key result
Mice harboring the Gata4G295Ski/wt mutation displayed functional semilunar valve stenosis predominantly affecting the aortic valve with severe extracellular matrix disorganization.
Authors
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Gata4 mutation models semilunar valve stenosis in mice; leaves open translation to human congenital valve therapies.
The Gata4G295S mutation in mice causes congenital semilunar valve stenosis characterized by ECM disorganization and EMT deficits, demonstrating a novel role for GATA4 in valve development.
LaHaye et al. (2019) studied Congenital heart disease (semilunar valve stenosis). Gata4G295Ski/wt mutation was evaluated on Semilunar valve development and stenosis. Mice harboring the Gata4G295Ski/wt mutation displayed functional semilunar valve stenosis predominantly affecting the aortic valve with severe extracellular matrix disorganization.