Key result
PI3Kgamma knockout in mouse hearts increased contractility and cAMP levels compared to wild-type controls, indicating PI3Kgamma reduces cAMP concentration independently of Gi-mediated signaling.
Population
Mouse heart preparations (PI3Kgamma-null mutants and wild-type controls)
Comparison
PI3Kgamma gene knockout (PI3Kgamma-null) vs Wild-type controls
Design
Preclinical
Authors
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May inform PI3Kgamma-targeted therapies for contractile dysfunction; leaves open translation from mouse models to human disease.
PI3Kgamma regulates cardiac function by reducing cAMP levels independently of Gi-mediated signaling.
Alloatti et al. (2004) studied Autonomic regulation of the mouse heart. PI3Kgamma knockout vs. Wild-type controls was evaluated on Cardiac contractility, heart rate, and cAMP levels. PI3Kgamma knockout in mouse hearts increased contractility and cAMP levels compared to wild-type controls, indicating PI3Kgamma reduces cAMP concentration independently of Gi-mediated signaling.
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