Why the study?
Does cardiac-specific expression of GRKnt reduce cardiac hypertrophy and prevent heart failure in mice after pressure overload?
Does cardiac-specific expression of GRKnt reduce cardiac hypertrophy and prevent heart failure in mice after pressure overload?
GRK5nt acts as an inhibitor of pathological GRK5 signaling, preventing heart failure in a mouse model of pressure overload.
GRK5nt may attenuate pressure-overload remodeling in mice; leaves open translation to human HF therapy.
-CaM from associating with endogenous GRK5, thereby preventing GRK5 nuclear accumulation after pressure overload. We generated mice that expressed GRKnt in a cardiac-specific fashion (TgGRK5nt mice), which exhibited reduced cardiac hypertrophy, ventricular dysfunction, pulmonary congestion, and cardiac fibrosis after chronic transverse aortic constriction. Together, our data support a role for GRK5nt as an inhibitor of pathological GRK5 signaling that prevents heart failure.
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Coleman et al. (2021) studied this question.
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