Key result
Cardiac-specific deletion of Gata4 in mice resulted in progressive deterioration in cardiac function, rapid decompensation following pressure overload, and compromised ability to hypertrophy.
Population
Gata4-loxP-targeted mice crossed with mice containing a beta-MHC or alpha-MHC promoter-driven Cre transgene
Design
Preclinical
Authors
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GATA4 is essential for adult cardiac compensation in mice; leaves open whether pathway modulation could influence human HF progression.
GATA4 is a necessary regulator of cardiac gene expression, hypertrophy, stress-compensation, and myocyte viability in the adult heart.
Oka et al. (2006) studied Cardiac hypertrophy and heart failure. Cardiac-specific deletion of Gata4 vs. Control mice was evaluated on Cardiac function, hypertrophy, and myocyte viability. Cardiac-specific deletion of Gata4 in mice resulted in progressive deterioration in cardiac function, rapid decompensation following pressure overload, and compromised ability to hypertrophy.
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