Key result
Inducible cardiomyocyte-specific inactivation of Gα13 protected mice from pressure overload-induced hypertrophy and fibrosis, and prevented heart failure up to 1 year after overloading.
Population
In vitro cell models and in vivo mouse models subjected to pressure overload
Comparison
siRNA-mediated knockdown in vitro and inducible… vs Control models and models with inactivation of Gα
Design
Preclinical
Follow-up
up to 1 year after overloading
Authors
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G13 signaling required for overload remodeling in models; leaves open whether targeting it prevents human HF progression.
The G12/13 family of heterotrimeric G proteins is centrally involved in pressure overload-induced cardiac remodeling and represents a potential mechanistic target for preventing heart failure.
Takefuji et al. (2012) studied Pressure overload-induced cardiac remodeling and heart failure. Inactivation of Gα13 vs. Control / Gα(q/11) inactivation was evaluated on Pressure overload-induced hypertrophy, fibrosis, and heart failure. Inducible cardiomyocyte-specific inactivation of Gα13 protected mice from pressure overload-induced hypertrophy and fibrosis, and prevented heart failure up to 1 year after overloading.
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