Key result
G alpha q plays a key role in the development of pressure overload cardiac hypertrophy and interacts with beta-adrenergic receptors, RGS proteins, and the proapoptotic factor Nix/Bnip3L.
This review summarizes the role of G alpha q and associated signaling pathways in the progression of cardiac hypertrophy to heart failure.
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No immediate clinical implications for hypertrophy; leaves open Gαq-targeted therapies for prospective validation.
Cardiac hypertrophy is an adaptive response to any cardiac insult or stress that increases hemodynamic load. Cardiac hypertrophy can exist in a state of compensation or progress to a decompensated state (i.e., heart failure) over time. It has been established through transgenic overexpression and gene ablation studies that multiple signaling pathways are involved in the induction of hypertrophy as well as its decompensation. This article reviews the role of G alpha q in the development of pressure overload hypertrophy and discusses the relationships between G alpha q and beta-adrenergic receptors, RGS proteins, and the proapoptotic factor, Nix/Bnip3L.
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Dorn et al. (2004) conducted a review in Cardiac hypertrophy. G alpha q was evaluated. G alpha q plays a key role in the development of pressure overload cardiac hypertrophy and interacts with beta-adrenergic receptors, RGS proteins, and the proapoptotic factor Nix/Bnip3L.
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