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 Gαq in the development of pressure overload hypertrophy and discusses the relationships between Gαq and β-adrenergic receptors, RGS proteins, and the proapoptotic factor, Nix/Bnip3L.

Original languageEnglish
Pages (from-to)225-237
Number of pages13
JournalAnnals of the New York Academy of Sciences
StatePublished - 2004


  • Heart failure
  • Myocardial hypertrophy
  • Receptor signaling


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