Key result
Disruption of glucocorticoid receptor in cardiomyocytes impaired foetal heart function, though unlike global GR knockout which had 22% reduced ventricular volume, SMGRKO heart size was normal.
Population
Mice with conditional disruption of glucocorticoid receptor in cardiomyocytes and vascular smooth muscle…
Comparison
Conditional disruption of glucocorticoid… vs Mice with global deficiency in GR (GR(-/-))
Design
Preclinical
Follow-up
Embryonic day (E)17.5
Authors
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Cardiomyocyte GR disruption impairs fetal cardiac function in mice; leaves open translation to human antenatal glucocorticoid effects or congenital heart disease.
Glucocorticoid signaling within cardiomyocytes and vascular smooth muscle is essential for structural and functional maturation of the fetal heart, although heart size regulation involves other pathways.
Rog‐Zielinska et al. (2013) studied Foetal heart maturation. Conditional disruption of glucocorticoid receptor (SMGRKO) vs. Global deficiency in GR (GR(-/-)) was evaluated on Heart function, cardiac ultrastructure, and ventricular volume. Disruption of glucocorticoid receptor in cardiomyocytes impaired foetal heart function, though unlike global GR knockout which had 22% reduced ventricular volume, SMGRKO heart size was normal.
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